The therapeutic benefits of opioids are compromised by the development of analgesic tolerance, which necessitates higher dosing for pain management thereby increasing the liability for drug dependence and addiction. Rodent models indicate opposing roles of the gut microbiota in tolerance: morphine-induced gut dysbiosis exacerbates tolerance, whereas probiotics ameliorate tolerance. Not all individuals develop tolerance, which could be influenced by differences in microbiota, and yet no study design has capitalized upon this natural variation. We leveraged natural behavioral variation in a murine model of voluntary oral morphine self-administration to elucidate the mechanisms by which microbiota influences tolerance. Although all mice shared similar morphine-driven microbiota changes that largely masked informative associations with variability in tolerance, our high-resolution temporal analyses revealed a divergence in the progression of dysbiosis that best explained sustained antinociception. Mice that did not develop tolerance maintained a higher capacity for production of the short-chain fatty acid (SCFA) butyrate known to bolster intestinal barriers and promote neuronal homeostasis. Both fecal microbial transplantation (FMT) from donor mice that did not develop tolerance and dietary butyrate supplementation significantly reduced the development of tolerance independently of suppression of systemic inflammation. These findings could inform immediate therapies to extend the analgesic efficacy of opioids.

Accelerated continuous theta burst stimulation (acTBS) is a more intensive and rapid protocol than continuous theta burst stimulation (cTBS). However, it remains uncertain whether acTBS exhibits anxiolytic effects. The aim of this study was to investigate the impact of acTBS on anxiety model mice and elucidate the underlying mechanisms involved, in order to provide a more comprehensive understanding of its effects.

Chronic restraint stress (CRS) model was employed to observe the anxiolytic effects of acTBS. The study focused on evaluating the impact of acTBS on behavior, neuroinflammation, gut and gut microbiota in mice with anxiety induced by CRS.

The application of acTBS ameliorated anxiety-like behaviors in CRS-induced mice. Notably, it effectively suppressed the activation of microglia and reduced the level pro-inflammatory cytokines in PFC, hippocampus, and amygdala of anxiety mice. Additionally, acTBS alleviated astrocyte activation specifically in hippocampus. The NF-κB signaling pathway involved in the anti-inflammatory effects of acTBS. Furthermore, acTBS ameliorated inflammation and histological damage in colon. 16S rRNA analysis revealed that acTBS significantly enhanced the relative abundance of Lactobacillus, while normalized the dysregulated levels of Coriobacterales, Bacteroides, and Parabacteroides caused by CRS. These changes facilitated chemoheterotrophic and fermentation functions within the microbiota. Importantly, changes in microbiota composition influenced by acTBS was found to be correlated with anxiety-like behaviors and neuroinflammation.

acTBS exerted anxiolytic effects on mice exposed to CRS, which was associated with the modulation of gut microbiota.

The gut microbiome has emerged as a novel and intriguing focus in mood disorder research. Emerging evidence demonstrates the significant role of the gut microbiome in influencing mental health, suggesting a bidirectional communication between the gut and the brain. This review examines the latest findings on the gut-microbiota-brain axis and elucidates how alterations in gut microbiota composition can influence this axis, leading to changes in brain function and behavior. Although dietary interventions, prebiotics, probiotics, and fecal microbiota transplantation have yielded encouraging results, significant advances are needed to establish next-generation approaches that precisely target the neurobiological mechanisms of mood disorders. Future research must focus on developing personalized treatments, facilitated by innovative therapies and technological progress, which account for individual variables such as age, sex, drug history, and lifestyle. Highlighting the potential therapeutic implications of targeting the gut microbiota, this review emphasizes the importance of integrating microbiota research into psychiatric studies to develop more effective and personalized treatment strategies for mood disorders.

Postpartum depressive symptoms (PDS) are a common mental health condition among women after delivery. Although various causative factors have been reported, PDS remains a challenging condition to predict and prevent. The disruption of the gut microbiota due to antibiotic exposure has been reported to affect psychiatric conditions. Similarly, previous research suggests that antibiotic exposure during pregnancy could be related to PDS. Therefore, this prospective study examines the association between antibiotic exposure during pregnancy and PDS for 6 months after delivery. Data were obtained from 65,272 mothers from the Japan environment and children's study, a prospective birth cohort study. The ratios of maternal PDS at 1 and 6 months after delivery were 12.3% and 10.1%, respectively. During pregnancy, 10.7% of women took antibiotics orally. Antibiotic exposure during pregnancy was associated with an increased risk of PDS only at 6 months after delivery (OR = 1.13, 95% CI [1.00, 1.26]), adjusted for potential confounding factors. An increase in Edinburgh Postnatal Depression Scale scores in relation to antibiotic exposure during pregnancy was primarily observed via psychological distress during pregnancy. Although a causal link was not established, antibiotic exposure during pregnancy may be a contributing risk factor for PDS. Therefore, when antibiotic administration is required, clinical practitioners and perinatal care providers should consider the potential risk for PDS.

The Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet is a novel dietary approach that exhibits neuroprotective benefits. Studies have found that the MIND diet can effectively reduce the risk of depression and anxiety, but the relationship between them is unclear among older Chinese people. The objective of this research was to explore the association of the MIND diet with depression and anxiety among elderly Chinese individuals.

The study data were obtained from the 2018 Chinese Longitudinal Healthy Longevity Survey (CLHLS), and logistic regression models were developed to explore the relationship between the Chinese version of MIND (cMIND) diet and depressive symptoms and anxiety symptoms. Restricted Cubic Spline (RCS) was used to determine whether a linear relationship exists between cMIND diet and depressive symptoms and anxiety symptoms. Subgroup and sensitivity analyses were further used to test for interactions and robustness of results.

The study included 6,945 Chinese seniors aged 65 and above, and the prevalence of depressive and anxiety symptoms were 49.68% and 10.89%, respectively. The cMIND diet score had a significant protective effect on both depressive and anxiety symptoms when used as a continuous or categorical variable. The RCS analysis revealed a statistically significant linear relationship between the cMIND diet and both depressive (p < 0.05) and anxiety symptoms (p < 0.05).

Among the Chinese elderly population, the cMIND diet can significantly reduce the probability of developing depressive and anxiety symptoms. Therefore, this study's results may promote healthy eating habits among the elderly.

Background/Objectives: Prenatal depression (PND) poses a significant threat to the health of both the mother and the developing fetus. Despite its increasing prevalence, the pathophysiology of PND is not yet fully elucidated. Methods: In this study, we aimed to investigate the fecal metabolites and gut microbiota in PND patients compared to healthy controls and to explore potential correlations between these factors. Results: Through untargeted metabolomics analysis, we identified 75 significantly altered metabolites in PND patients, of which 27 were structurally annotated and implicated key pathways, such as linoleic acid metabolism and phenylalanine, tyrosine, and tryptophan biosynthesis. Notably, two Clostridia-associated enterobacteria, unclassified_c_Clostridia and unclassified_f_Lachnospiraceae, which were enriched in the PND group, were significantly positively correlated with tyrosine and negatively correlated with multiple sulfated neurosteroids. Conclusions: Our findings underscore a robust association between gut microbiota dysbiosis and metabolic disturbances in PND, with specific alterations noted in tyrosine metabolism, sulfated neurosteroid homeostasis, and linoleic acid pathways. These dysregulated metabolites-tyrosine, sulfated neurosteroids, and linoleic acid-may serve as potential diagnostic biomarkers and therapeutic targets. Moreover, their interplay provides new insights into the pathophysiological mechanisms of PND, particularly highlighting the role of gut-brain axis signaling in neuroendocrine dysregulation and inflammatory responses. However, further large-scale studies and animal models are required to validate these findings and explore detailed mechanistic pathways.

The gut microbiome plays a fundamental role in mental health, influencing mood, cognition, and emotional regulation through the gut-brain axis. This bidirectional communication system connects the gastrointestinal and CNS, facilitated by microbial metabolites, neurotransmitters, and immune interactions. Recent research highlights the association between gut dysbiosis and psychiatric disorders, including anxiety, depression, and stress-related conditions. Key findings indicate that altered microbial diversity, decreased short-chain fatty acid (SCFA) production, and increased neuroinflammation contribute to mental health disturbances. This paper explores the mechanism linking the gut microbiome to brain function, including microbial neurotransmitter synthesis, vagus nerve signaling, and hypothalamic-pituitary-adrenal (HPA) axis modulation. Additionally, it evaluates the potential of microbiome-targeted interventions, such as probiotics, prebiotics, dietary modifications, and fecal microbiota transplantation (FMT), in alleviating psychiatric symptoms. Microbiome sequencing and bioinformatics advances further support the development of personalized microbiome-based mental health interventions. Despite promising evidence, challenges such as inter-individual variability, methodological inconsistencies, and the need for longitudinal studies remain. Future research should focus on standardizing microbiome assessment techniques and optimizing therapeutic applications. Integrating precision psychiatry with microbiome-based diagnostics holds immense potential in transforming mental health treatment.

The gut and brain interact through various metabolic and signaling pathways, each of which influences mental health. Gut dysbiosis caused by antibiotics is a well-known phenomenon that has serious implications for gut microbiota-brain interactions. Although antibiotics disrupt the gut microbiota's fundamental structure, the mechanisms that modulate the response and their impact on brain function are still unclear. It is imperative to comprehend and investigate crucial regulators and factors that play important roles. We aimed to study the effect of long-term antibiotic-induced disruption of gut microbiota, host metabolomes, and brain function and, particularly, to determine the basic interactions between them by treating the C57BL/6 mice with two different, most commonly used antibiotics, ciprofloxacin and amoxicillin. Anxiety-like behavior was confirmed by the elevated plus-maze test and open field test. Gut microbes and their metabolite profiles in fecal, serum, and brain samples were determined by 16S rRNA sequencing and untargeted metabolomics. In our study, long-term antibiotic treatment exerted anxiety-like effects. The fecal microbiota and metabolite status revealed that the top five genera found were Lactobacillus, Bacteroides, Akkermansia, Ruminococcus_gnavus_group, and unclassified norank_f_Muribaculaceae. The concentration of serotonin, L-Tyrosine, 5-Hydroxy-L-tryptophan, L-Glutamic acid, L-Glutamate, 5-Hydroxyindole acetic acid, and dopaminergic synapsis was comparatively low, while adenosine was high in antibiotic-treated mice. The KEGG enrichment analysis of serum and brain samples showed that amino acid metabolism pathways, such as tryptophan metabolism, threonine metabolism, serotonergic synapsis, methionine metabolism, and neuroactive ligand-receptor interaction, were significantly decreased in antibiotic-treated mice. Our study demonstrates that long-term antibiotic use induces gut dysbiosis and alters metabolic responses, leading to the dysregulation of brain signaling molecules and anxiety-like behavior. These findings highlight the complex interactions between gut microbiota and metabolic functions, providing new insights into the influence of microbial communities on gut-brain communication.

Mental health issues, particularly anxiety and depression, are increasingly prevalent among the occupational population. Environmental factors, such as dust exposure, may contribute to the worsening of these symptoms. While previous studies have examined the association between dust exposure and mental health, the moderating effect of sleep duration on this link in occupational settings remains under-explored.

This study was conducted from July to October 2023 at The Fifth People's Hospital of Ningxia and recruited dust-expose d occupational workers from different coal enterprises. After a series of screening 1274 valid subjects were finally included. Binary logistic regression was used to explore the association of dust exposure with anxiety and depression. Generalized additive models (GAM) were constructed to explore the nonlinear relationships between dust exposure duration, sleep duration, and mental health outcomes. Mediating variable contributions were isolated using the Karlson-Holm-Breen (KHB) method and mediated effects models were fitted.

The prevalence of anxiety and depression was found to be 6.44% and 4.24%, respectively. Dust exposure duration was positively associated with both anxiety and depression, while stratification by monthly income level had no significant effect. The contribution of sleep duration to the indirect effect accounted for 21.76% and 43.54% of the total effect of dust exposure duration on anxiety and depression scores, respectively. A nonlinear relationship was observed between dust exposure duration, sleep duration, and the scores of anxiety and depression. In the mediation analysis, shorter sleep duration explained 12.87% of the association between dust exposure duration and anxiety scores.

Dust exposure duration was associated with anxiety and depression, with a nonlinear relationship between them. Changes in sleep duration may effectively influence mental health problems in occupationally dust-exposed populations.

The global incidence and burden of Major Depressive Disorder (MDD) are increasing annually, with current antidepressant treatments proving ineffective for 30-40% of patients. Biomolecular mechanisms within the microbiota-gut-brain axis (MGBA) may significantly contribute to MDD, potentially paving the way for novel treatment approaches. However, integrating the MGBA with the psychological and environmental aspects of MDD remains challenging. This manuscript aims to: 1) investigate the underlying biomolecular mechanisms of MDD using a modeling approach, and 2) integrate this knowledge into a comprehensive 'spiraling risk factor model' to develop a biopsychosocial translational research framework for the prevention and treatment of MDD.

For the first aim, a systematic review (PROSPERO registration) was conducted using PubMed, Embase, and Scopus to query literature published between 2016-2020, with select additional sources. A narrative review was performed for the second aim.

In addition to genetics and neurobiology, research consistently indicates that hyperactivation of the HPA axis and a pro-inflammatory state are interrelated components of the MGBA and likely underlying mechanisms of MDD. Dysregulation of the MGBA, along with imbalances in mental and physical conditions, lifestyle factors, and pre-existing treatments, can trigger a downward spiral of stress and anxiety, potentially leading to MDD.

MDD is not solely a brain disorder but a heterogeneous condition involving biomolecular, psychological, and environmental risk factors. Future interdisciplinary research can utilize the integrated biopsychosocial insights from this manuscript to develop more effective lifestyle-focused multimodal treatment interventions, enhance diagnosis, and stimulate early-stage prevention of MDD.

https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42020215412.

Dietary fibers hold potential to influence depressive and anxiety outcomes by modulating the microbiota-gut-brain axis, which is increasingly recognized as an underlying factor in mental health maintenance.

Evidence for the effects of fibers on depressive and anxiety outcomes remains unclear. To this end, a systematic literature review and a meta-analysis were conducted that included observational studies and randomized controlled trials (RCTs).

The PubMed, Embase, CENTRAL, CINAHL, and PsychINFO databases were searched for eligible studies.

Study screening and risk-of-bias assessment were conducted by 2 independent reviewers.

Meta-analyses via random effects models were performed to examine the (1) association between fiber intake and depressive and anxiety outcomes in observational studies, and (2) effect of fiber intervention on depressive and anxiety outcomes compared with placebo in RCTs. A total of 181 405 participants were included in 23 observational studies. In cross-sectional studies, an inverse association was observed between fiber intake and depressive (Cohen's d effect size [d]: -0.11; 95% confidence interval [CI]: -0.16, -0.05) and anxiety (d = -0.25; 95%CI, -0.38, -0.12) outcomes. In longitudinal studies, there was an inverse association between fiber intake and depressive outcomes (d = -0.07; 95%CI, -0.11, -0.04). In total, 740 participants were included in 10 RCTs, all of whom used fiber supplements. Of note, only 1 RCT included individuals with a clinical diagnosis of depression. No difference was found between fiber supplementation and placebo for depressive (d = -0.47; 95%CI, -1.26, 0.31) or anxiety (d = -0.30; 95%CI, -0.67, 0.07) outcomes.

Although observational data suggest a potential benefit for higher fiber intake for depressive and anxiety outcomes, evidence from current RCTs does not support fiber supplementation for improving depressive or anxiety outcomes. More research, including RCTs in clinical populations and using a broad range of fibers, is needed.

PROSPERO registration no. CRD42021274898.

This review article investigates the intricate relationship between nutrigenomics and neurological disorders, highlighting how genetic variations affect an individual's response to nutrients. The study delves into the role of diet-related oxidative stress and the gut-brain axis in the progression and management of brain disorders such as Parkinson's disease, Alzheimer's disease, epilepsy, stroke, migraines, and depression. The review encompasses various clinical trials and introduces new trends and techniques, including omics and artificial intelligence, in identifying and managing neurological disorders. The main findings emphasize that personalized diet recommendations, tailored to an individual's genetic makeup, can significantly improve cognitive health and manage neurological conditions. The study concludes that further research in the field of nutrigenomics is essential to advancing personalized nutrition strategies for better neurological functioning, ultimately linking diet, genes, and brain health.

Chronic exposure to glucocorticoids in response to long-term stress is thought to be a risk factor for major depression. Depression is associated with disturbances in the gut microbiota composition and peripheral and central energy metabolism. However, the relationship between chronic glucocorticoid exposure, the gut microbiota, and brain metabolism remains largely unknown. In this study, we first investigated the effects of chronic corticosterone exposure on various domains of behavior in adult male C57BL/6J mice treated with the glucocorticoid corticosterone to evaluate them as an animal model of depression. We then examined the gut microbial composition and brain and plasma metabolome in corticosterone-treated mice. Chronic corticosterone treatment resulted in reduced locomotor activity, increased anxiety-like and depression-related behaviors, decreased rotarod latency, reduced acoustic startle response, decreased social behavior, working memory deficits, impaired contextual fear memory, and enhanced cued fear memory. Chronic corticosterone treatment also altered the composition of gut microbiota, which has been reported to be associated with depression, such as increased abundance of Bifidobacterium, Turicibacter, and Corynebacterium and decreased abundance of Barnesiella. Metabolomic data revealed that long-term exposure to corticosterone led to a decrease in brain neurotransmitter metabolites, such as serotonin, 5-hydroxyindoleacetic acid, acetylcholine, and gamma-aminobutyric acid, as well as changes in betaine and methionine metabolism, as indicated by decreased levels of adenosine, dimethylglycine, choline, and methionine in the brain. These results indicate that mice treated with corticosterone have good face and construct validity as an animal model for studying anxiety and depression with altered gut microbial composition and brain metabolism, offering new insights into the neurobiological basis of depression arising from gut-brain axis dysfunction caused by prolonged exposure to excessive glucocorticoids.

In this study, we aimed to evaluate the relationship between the dietary inflammatory index (DII) and mental health outcomes among patients with migraine headaches.

In this cross-sectional study, 262 subjects were included. The dietary intakes were collected using a validated 168-item semi-quantitative food frequency questionnaire. Items were scored according to their inflammatory potential, so a higher DII indicated a more pro-inflammatory diet. The association between DII and the mental health of participants was investigated using multinomial logistic regression and odds ratio (OR) with a corresponding 95% confidence interval (CI) was reported.

Overall, 224 women and 38 men, with a mean (standard error) DII of -2.96 (0.06), age of 36.1 (0.53) years, and BMI of 25.55 (0.21) kg/m2, comprised our study population. DII was positively associated with a higher risk of depression in patients with the highest adherence to a pro-inflammatory diet compared to those with the lowest adherence (OR = 1.76; 95%CI: 1.04, 3.00; Ptrend = 0.035). Adjustments for age, sex, marital status, smoking status, migraine headache index score, number of family members, mean arterial pressure, medication, physical activity, and BMI intensified the association in a way that the risk of depression was 2.03 times higher in patients with the highest adherence to a pro-inflammatory diet compared to those with the lowest adherence to a pro-inflammatory diet (OR = 2.03; 95%CI: 1.18, 3.49; Ptrend = 0.011).

Our findings suggest that depression was positively associated with adherence to a pro-inflammatory diet. However, no significant association was observed between anxiety and stress with DII.

The gut-brain axis plays an important role in mental health. The intestinal epithelial surface is colonized by billions of commensal and transitory bacteria, known as the Gut Microbiota (GM). However, potential pathogens continuously stimulate intestinal immunity when they find the place. The last two decades have witnessed several studies revealing intestinal bacteria as a key factor in the health-disease balance of the gut, as well as disease-emergent in other parts of the body. Various neurological processes, such as cognition, learning, and memory, could be affected by dysbiosis in GM. Additionally, the aging process and longevity are related to systemic inflammation caused by dysbiosis. Commensal GM affects brain development, behavior, and healthy aging suggesting that building changes in GM might be a potential therapeutic method. The innovation in GM dysbiosis is intervention by Fecal Microbiota Transplantation (FMT), which has been confirmed as a therapy for recurrent Clostridium difficile infections and is promising for other clinical disorders, such as Parkinson's disease, Multiple Sclerosis (MS), Alzheimer's disease, and depression. Additionally, FMT may be possible to promote healthy aging, and extend longevity. This review aims to connect dysbiosis, neurological disorders, and aging and the potential of FMT as a therapeutic strategy to treat these disorders, and to enhance the quality of life in the elderly.

The therapeutic potential of yeast in the management of depression is unknown. Thus, we evaluated the modulatory effect of nutritional yeast supplementation on antidepressant activity of fluoxetine in mice models of depressive-like behaviors (DLB).

A total of 112 mice were divided into 16 groups (n = 7 each) for a 3-stage study. Stage I (non-DLB study) had groups Ia (10 mL/kg vehicle), Ib (20 mg/kg fluoxetine), Ic - If (2% yeast diet for all, but Id - If additionally received 5 mg/kg, 10 mg/kg, and 20 mg/kg fluoxetine respectively). Stage II (lipopolysaccharide [LPS] model of DLB) had groups IIa - IIb (10 mL/kg vehicle), IIc (20 mg/kg fluoxetine), IId (yeast) and IIe (yeast + 20 mg/kg fluoxetine). After these treatments for 24 days, animals in IIb - IIe received 0.83 mg/kg of LPS on the 25th day. Except for group IIIa (10 mL/kg vehicle), animals in other groups of stage III (unpredictable chronic mild stress [UCMS] model) were exposed to UCMS for 24 days along with 10 mL/kg vehicle (IIIb), 20 mg/kg fluoxetine (IIIc), yeast (IIId), or yeast + fluoxetine (IIIe).

Yeast and fluoxetine attenuated LPS- and UCMS-induced immobility, derangement of oxido-inflammatory (TNF-α, IL-6, NO, MDA, SOD, GSH, CAT, and AChE) and CREB/MAPK pathways. While fluoxetine had more potent effect than yeast when used separately, pre-treatment of mice with their combination had more pronounced effect than either of them.

Yeast supplementation improves the antidepressant activity of fluoxetine in mice by modulating oxido-inflammatory, CREB, and MAPK pathways.

Clinical mental health researchers may understandably struggle with how to incorporate biological assessments in clinical research. The options are numerous and are described in a vast and complex body of literature. Here we provide guidelines to assist mental health researchers seeking to include biological measures in their studies. Apart from a focus on behavioral outcomes as measured via interviews or questionnaires, we advocate for a focus on biological pathways in clinical trials and epidemiological studies that may help clarify pathophysiology and mechanisms of action, delineate biological subgroups of participants, mediate treatment effects, and inform personalized treatment strategies. With this paper we aim to bridge the gap between clinical and biological mental health research by (1) discussing the clinical relevance, measurement reliability, and feasibility of relevant peripheral biomarkers; (2) addressing five types of biological tissues, namely blood, saliva, urine, stool and hair; and (3) providing information on how to control sources of measurement variability.

Alzheimer's disease (AD) is a complex neurodegenerative condition with growing evidence implicating the gut microbiota in its pathogenesis. This study aimed to investigate the effects of NMN synbiotics, a combination of β-nicotinamide mononucleotide (NMN), Lactobacillus plantarum, and lactulose, on the gut microbiota composition and metabolic profiles in APP/PS1 transgenic mice. Results demonstrated that NMN synbiotics led to a notable restructuring of the gut microbiota, with a decreased Firmicutes/Bacteroidetes ratio in the AD mice, suggesting a potential amelioration of gut dysbiosis. Alpha diversity indices indicated a reduction in microbial diversity following NMN synbiotics supplementation, while beta diversity analyses revealed a shift towards a more balanced microbial community structure. Functional predictions based on the 16S rRNA data highlighted alterations in metabolic pathways, particularly those related to amino acid and energy metabolism, which are crucial for neuronal health. The metabolomic analysis uncovered a significant impact of NMN synbiotics on the gut metabolome, with normalization of metabolic composition in AD mice. Differential metabolite functions were enriched in pathways associated with neurotransmitter synthesis and energy metabolism, pointing to the potential therapeutic effects of NMN synbiotics in modulating the gut-brain axis and synaptic function in AD. Immunohistochemical staining observed a significant reduction of amyloid plaques formed by Aβ deposition in the brain of AD mice after NMN synbiotics intervention. The findings underscore the potential of using synbiotics to ameliorate the neurodegenerative processes associated with Alzheimer's disease, opening new avenues for therapeutic interventions.

One of the most challenging and controversial issues in microbiome research is related to gut microbial metabolism and neuropsychological disorders. Psychobiotics affect human behavior and central nervous system processes via the gut-brain axis, involving neuronal, immune, and metabolic pathways. They have therapeutic potential in the treatment of several neurodegenerative and neurodevelopmental disorders such as depression, anxiety, autism, attention deficit hyperactivity disorder, Alzheimer's disease, Parkinson's disease, schizophrenia, Huntington's disease, anorexia nervosa, and multiple sclerosis. However, the mechanisms underlying the interaction between psychobiotics and the abovementioned diseases need further exploration. This review focuses on the relationship between gut microbiota and its impact on neurological and neurodegenerative disorders, examining the potential of psychobiotics as a preventive and therapeutic approach, summarising recent research on the gut-brain axis and the potential beneficial effects of psychobiotics, highlighting the need for further research and investigation in this area.

Depression post-myocardial infarction (MI) is becoming more prevalent. The gut-brain axis (GBA), influenced by the gut microbiota, is a critical component in understanding depression post-MI. Despite the well-established connection between gut microbiota and depression post-MI, this relationship remains incompletely understood.

This protocol will follow the Preferred Reporting Items for Systematic Review and Meta-analysis Protocol (PRISMA-P) 2020 statement. Beginning from inception to October 2023, a systematic search will be conducted across eight electronic databases, including PubMed, MEDLINE, Scopus, Embase, Cochrane Clinical Trials Database, Web of Science, China National Knowledge Infrastructure, and China Biomedical Literature Database. Pre-selected studies will be independently assessed by two researchers following a standard inclusion, data extraction and quality assessment protocol. The primary outcome measures are differences in the profile of gut microbiota and rating scale scores for depression. Fixed-effects models will be used when both clinical heterogeneity and statistical heterogeneity are low, otherwise random-effects models will be used. Furthermore, subgroup analyses will be conducted on the depression severity of the participants using the same psychiatric scales employed, study type and geographic region. Random forest plot runs and research-related statistical analyses will be carried out using Rev Man V.5.3 software.

This study will identify the association between the gut microbiota and the onset of depression post-MI, and provide evidence for the use of probiotics as an adjunctive treatment for depression post-MI.

Prospero registration number: CRD42023444026.

Dietary components, including dietary fiber, unsaturated fatty acids, and polyphenols, along with meal timing and spacing, significantly affect the microbiota's capacity to produce various metabolites essential for quality sleep and overall health. This review explores the role of gut microbiota in regulating sleep through various metabolites such as short-chain fatty acids, tryptophan, serotonin, melatonin, and gamma-aminobutyric acid. A balanced diet rich in plant-based foods enhances the production of these sleep-regulating metabolites, potentially benefiting overall health. This review aims to investigate how dietary habits affect gut microbiota composition, the metabolites it produces, and the subsequent impact on sleep quality and related health conditions.

The role of the gut microbiota in the pathophysiology of depression has been explored in numerous studies, which have confirmed that the baseline gut microbial profiles of patients with depression differ from those of healthy individuals. The gut microbiome affects metabolic activity in the immune and central nervous systems and regulates intestinal ecology through the neuroendocrine system. Additionally, baseline changes in the gut microbiota differed among patients with depression who demonstrated varying treatment response. Currently, probiotics are an emerging treatment for depression; however, the efficacy of modulating the gut microbiota in the treatment of depression remains uncertain. Additionally, the mechanisms by which changes in the gut microbiota affect treatment response in patients with depression remain unclear. In this review, we aimed to summarize the differences in the baseline gut microbiota between the remission and non-remission groups after antidepressant therapy. Additionally, we summarized the possible mechanisms that may contribute to antidepressant resistance through the effects of the gut microbiome on the immune and nervous systems, various enzymes, bioaccumulation, and blood-brain barrier, and provide a basis for treating depression by targeting the gut microbiota.

Despite mounting evidence of gut-brain involvement in psychiatric conditions, functional data remain limited, and analyses of other microbial niches, such as the vaginal microbiota, are lacking in relation to mental health. This aim of this study was to investigate if the connections between the gut microbiome and mental health observed in populations with a clinical diagnosis of mental illness extend to healthy women experiencing stress and depressive symptoms. Additionally, this study examined the functional pathways of the gut microbiota according to the levels of psychological symptoms. Furthermore, the study aimed to explore potential correlations between the vaginal microbiome and mental health parameters in young women without psychiatric diagnoses.

In this cross-sectional study, 160 healthy Danish women (aged 18-40 years) filled out questionnaires with validated scales measuring symptoms of stress and depression and frequency of dietary intake. Fecal and vaginal microbiota samples were collected at the beginning of the menstrual cycle and vaginal samples were also collected at cycle day 8-12 and 18-22. Shotgun metagenomic profiling of the gut and vaginal microbiome was performed. The Kyoto Encyclopedia of Genes and Genomes (KEGG) was used for functional profiling and 56 Gut Brain Modules were analyzed in the fecal samples.

The relative abundance in the gut of the genera Escherichia, Parabacteroides, and Shigella was higher in women with elevated depressive symptoms. Women with high perceived stress showed a tendency of increased abundance of Escherichia, Shigella, and Blautia. Amongst others, the potentially pathogenic genera, Escherichia and Shigella correlate with alterations in the neuroactive pathways such as the glutamatergic, GABAeric, dopaminergic, and Kynurenine pathways. Vaginosis symptoms were more prevalent in women reporting high levels of stress and depressive symptoms.

The findings of this study support the concept of a microbiota-associated effect on the neuroactive pathways even in healthy young women. This suggest, that targeting the gut microbiome could be a promising approach for future psychiatric interventions.

Interactions between the gut microbiota and host immunity are sophisticated, dynamic, and host-dependent. Scientists have recently conducted research showing that disturbances in the gut bacterial community can lead to a decrease in some metabolites and, consequently, to behaviors such as depression. Exposure to stressors dropped the relative abundance of bacteria in the genus Bacteroides while soaring the relative abundance of bacteria in the genus Clostridium, Coprococcus, Dialister, and Oscillibacter, which were also reduced in people with depression. Microbiota and innate immunity are in a bilateral relationship. The gut microbiota has been shown to induce the synthesis of antimicrobial proteins such as catalysidins, type C lectins, and defensins. Probiotic bacteria can modulate depressive behavior through GABA signaling. The gut microbiome produces essential metabolites such as neurotransmitters, tryptophan metabolites, and short-chain fatty acids (SCFAs) that can act on the CNS. In the case of dysbiosis, due to mucin changes, the ratio of intestinal-derived molecules may change and contribute to depression. Psychotropics, including Bifidobacterium longum NCC3001, Clostridium butyricum CBM588, and Lactobacillus acidophilus, have mental health benefits, and can have a positive effect on the host-brain relationship, and have antidepressant effects. This article reviews current studies on the association between gut microbiota dysbiosis and depression. Comprehensively, these findings could potentially lead to novel approaches to improving depressive symptoms via gut microbiota alterations, including probiotics, prebiotics, and fecal microbiota transplantation.

The gastrointestinal (GI) tract harbors trillions of microorganisms known to influence human health and disease, and next-generation sequencing (NGS) now enables the in-depth analysis of their diversity and functions. Although a significant amount of research has been conducted on the GI microbiome, comprehensive metagenomic datasets covering the entire tract are scarce due to cost and technical challenges. Despite the widespread use of fecal samples, integrated datasets encompassing the entire digestive process, beginning at the mouth and ending with feces, are lacking. With this study, we aimed to fill this gap by analyzing the complete metagenome of the GI tract, providing insights into the dynamics of the microbiota and potential therapeutic avenues. In this study, we delved into the complex world of the GI microbiota, which we examined in five healthy Japanese subjects. While samples from the whole GI flora and fecal samples provided sufficient bacteria, samples obtained from the stomach and duodenum posed a challenge. Using a principal coordinate analysis (PCoA), clear clustering patterns were identified; these revealed significant diversity in the duodenum. Although this study was limited by its small sample size, the flora in the overall GI tract showed unwavering consistency, while the duodenum exhibited unprecedented phylogenetic diversity. A visual heat map illustrates the discrepancy in abundance, with Fusobacteria and Bacilli dominating the upper GI tract and Clostridia and Bacteroidia dominating the fecal samples. Negativicutes and Actinobacteria were found throughout the digestive tract. This study demonstrates that it is possible to continuously collect microbiome samples throughout the human digestive tract. These findings not only shed light on the complexity of GI microbiota but also provide a basis for future research.

This review offers a comprehensive evaluation of current aspects related to nutritional strategies, brain modulation, and muscle recovery, focusing on their applications and the underlying mechanisms of physiological adaptation for promoting a healthy brain, not only in athletes but also for recreationally active and inactive individuals. We propose that applying the rule, among others, of good sleep, regular exercise, and a properly balanced diet, defined as "SPARKS", will have a beneficial effect on the function and regeneration processes of the gut-brain-muscle axis. However, adopting the formula, among others, of poor sleep, stress, overtraining, and dysbiosis, defined as "SMOULDER", will have a detrimental impact on the function of this axis and consequently on human health as well as on athletes. Understanding these dynamics is crucial for optimizing brain health and cognitive function. This review highlights the significance of these factors for overall well-being, suggesting that adopting the "SPARKS" approach may benefit not only athletes but also older adults and individuals with health conditions.

This study attempted to analyze the effect of supplementing Wistar-Kyoto rats with fermented milk containing the probiotic Bifidobacterium animalis BB-12 and pomegranate juice on the microbiota-gut-brain axis of rats, with special focus on their behavior, sleep patterns, and response to stress. This study was divided into two experiments: (1) For the behavioral analysis the animals were divided into two groups: Fermented probiotic milk (BB + 1) and control (BB-). (2) For the sleep analysis the animals were divided into two groups: Fermented probiotic milk (BB + 2) and control (H2O). For the behavioral analysis, the open field method was used, which evaluates the behavior after ten, twenty, and thirty days of supplementation. For sleep analysis, the animals were submitted to implantation of electrodes and 24 h polysomnography, followed by 48 h sleep deprivation (REM) and 48 h polysomnography, then euthanized 100 days after the beginning of the experiment. In addition, animal feces were collected before and after sleep deprivation to assess its effects on the microbiota. A decrease in anxiety-related behaviors was observed in the supplemented animals and an increase in sleep efficiency and a reduction in the number of awakenings of the animals before deprivation. It has also been observed that sleep deprivation decreased the amount of total bacterial DNA. The number of copies of genomes of the genus Bifidobacterium did not differ in both groups.

Negative emotions and gut microbiota during pregnancy both bear significant public health implications. However, the relationship between them has not been fully elucidated. This study, utilizing data from a pregnancy cohort, employed metagenomic sequencing to elucidate the relationship between anxiety, depression, and gut microbiota's diversity, composition, species, and functional pathways. Data from 87 subjects, spanning 225 time points across early, mid, and late pregnancy, were analyzed. The results revealed that anxiety and depression significantly corresponded to lower alpha diversity (including the Shannon entropy and the Simpson index). Anxiety and depression scores, along with categorical distinctions of anxiety/non-anxiety and depression/non-depression, were found to account for 0.723%, 0.731%, 0.651%, and 0.810% of the variance in gut-microbiota composition (p = 0.001), respectively. Increased anxiety was significantly positively associated with the abundance of Oscillibacter sp. KLE 1745, Oscillibacter sp. PEA192, Oscillibacter sp. KLE 1728, Oscillospiraceae bacterium VE202 24, and Treponema socranskii. A similar association was significantly noted for Oscillibacter sp. KLE 1745 with elevated depression scores. While EC.3.5.3.1: arginase appeared to be higher in the anxious group than in the non-anxious group, vitamin B12-related enzymes appeared to be lower in the depression group than in the non-depression group. The changes were found to be not statistically significant after post-multiple comparison adjustment.

Melatonin is a highly conserved molecule produced in the human pineal gland as a hormone. It is known for its essential biological effects, such as antioxidant activity, circadian rhythm regulator, and immunomodulatory effects. The gut is one of the primary known sources of melatonin. The gut microbiota helps produce melatonin from tryptophan, and melatonin has been shown to have a beneficial effect on gut barrier function and microbial population. Dysbiosis of the intestinal microbiota is associated with bacterial imbalance and decreased beneficial microbial metabolites, including melatonin. In this way, low melatonin levels may be related to several human diseases. Melatonin has shown both preventive and therapeutic effects against various conditions, including neurological diseases such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. This review was aimed to discuss the role of melatonin in the body, and to describe the possible relationship between gut microbiota and melatonin production, as well as the potential therapeutic effects of melatonin on neurological diseases.

Shift work can disrupt sleep quality and gut health. Nurses and midwives constitute approximately half of the global healthcare shift-working workforce. Our previous study revealed that most midwives were experiencing suboptimal health conditions, characterized by poor sleep quality and a high prevalence of gastrointestinal diseases. The gut-brain axis theory highlights the potential interplay between sleep quality and gut health. However, limited research focuses on this relationship among midwives.

A cross-sectional survey included 2041 midwives from 87 Chinese hospitals between March and October 2023. Participants completed standardized questionnaires assessing sleep quality, gut health, depression, anxiety, and work stress. Binary logistic regression analyzed factors associated with poor sleep, and multiple linear regression examined the influence of sleep quality on gut health.

Over 60% of midwives reported poor sleep, with many experiencing gastrointestinal disorders. We observed a bidirectional relationship between sleep quality and gut health among midwives. After multivariable adjustments, midwives with higher gut health scores were more likely to experience poor sleep quality (odds ratio = 1.042, 95% confidence interval = 1.03-1.054). Conversely, midwives with higher sleep quality scores were also more likely to have poor gut health (β = 0.222, 95% confidence interval = 0.529-0.797). These associations remained robust across sensitivity analyses. Furthermore, depression, anxiety, and work stress significantly affected both sleep quality and gut health among midwives.

This study enhances our understanding of the intricate relationship between sleep quality and gut health among midwives. Poor gut health was associated with a higher risk of poor sleep, and vice versa. To improve the overall wellbeing of midwives, the findings emphasize the importance of addressing poor sleep quality and promoting gut health through maintaining a healthy diet, lifestyle, and good mental health. Further studies are needed to confirm our findings and clarify the underlying mechanisms.

The use of emulsion gels to protect and deliver probiotics has become an important topic in the food industry. This study used transglutaminase (TGase) to regulate ovalbumin (OVA) to prepare a novel emulsion gel. The effects of OVA concentration and the addition of TGase on the microstructure, rheological properties, water-holding capacity, and stability of the emulsion gels were investigated.

With the addition of TGase and the increasing OVA, the particle size of the emulsion gels decreased significantly (P < 0.05). The gels with TGase exhibited greater water holding, hardness, and chewiness to some extent by forming a more uniform and stable system. After simulated digestion, the survival rate of Bifidobacterium lactis embedded in OVA emulsion gels improved significantly in comparison with the oil-water mixture as a result of the protective effect of the emulsion gel encapsulation.

By increasing the OVA content and adding TGase, the rheological characteristics, stability, and encapsulation capability of the OVA emulsion gel could be enhanced, providing a theoretical basis for the use of emulsion gels to construct probiotic delivery systems. © 2023 Society of Chemical Industry.

The pathophysiology of functional bowel disorders is complex, involving disruptions in gut motility, visceral hypersensitivity, gut-brain-microbiota interactions, and psychosocial factors. Light pollution, as an environmental stressor, has been associated with disruptions in circadian rhythms and the aggravation of stress-related conditions. In this study, we investigated the effects of environmental stress, particularly continuous light exposure, on intestinal motility and inflammation using zebrafish larvae as a model system. We also evaluated the efficacy of probiotics, specifically Bifidobacterium longum (B. longum), at alleviating stress-induced constipation. Our results showed that continuous light exposure in zebrafish larvae increased the cortisol levels and reduced the intestinal motility, establishing a stress-induced-constipation model. We observed increased inflammatory markers and decreased intestinal neural activity in response to stress. Furthermore, the expressions of aquaporins and vasoactive intestinal peptide, crucial for regulating water transport and intestinal motility, were altered in the light-induced constipation model. Administration of probiotics, specifically B. longum, ameliorated the stress-induced constipation by reducing the cortisol levels, modulating the intestinal inflammation, and restoring the intestinal motility and neural activity. These findings highlight the potential of probiotics to modulate the gut-brain axis and alleviate stress-induced constipation. Therefore, this study provides a valuable understanding of the complex interplay among environmental stressors, gut function, and potential therapeutic strategies.

Alcohol use disorder (AUD) represents a major public health issue which affects millions of people globally and consist a chronic relapsing condition associated with substantial morbidity and mortality. The gut microbiome plays a crucial role in maintaining overall health and has emerged as a significant contributor to the pathophysiology of various psychiatric disorders. Recent evidence suggests that the gut microbiome is intimately linked to the development and progression of AUD, with alcohol consumption directly impacting its composition and function. This review article aims to explore the intricate relationship between the gut microbiome and AUD, focusing on the implications for mental health outcomes and potential therapeutic strategies. We discuss the bidirectional communication between the gut microbiome and the brain, highlighting the role of microbiota-derived metabolites in neuroinflammation, neurotransmission, and mood regulation. Furthermore, we examine the influence of AUD-related factors, such as alcohol-induced gut dysbiosis and increased intestinal permeability, on mental health outcomes. Finally, we explore emerging therapeutic avenues targeting the gut microbiome in the management of AUD, including prebiotics, probiotics, and fecal microbiota transplantation. Understanding the complex interplay between the gut microbiome and AUD holds promise for developing novel interventions that could improve mental health outcomes in individuals with AUD.