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Nutrient-Synbiotic Complex Ameliorates LPS-Induced Depressive-Like Behavior via Modulation of Gut Microbiota and Tryptophan Metabolism in Mice.
The conventional antidepressant treatments are ineffective, having undesirable side effects and relapse susceptibility. Nutrient and probiotics supplementation may have adjuvant antidepressant effects. This study aims to develop and assess the antidepressant properties of a nutrient-synbiotic complex and investigate the underlying mechanisms. We randomly divided into control, model, and four complex groups (nutrient, prebiotic, probiotic and united all components, respectively). We used lipopolysaccharide (LPS) to establish the depression model and assessed depressive-like behaviors using various behavioral tests, neuroplasticity, tryptophan pathway metabolites, and brain-derived neurotrophic factor (BDNF) in serum and prefrontal cortex (PFC). Intestinal microbiome analysis was performed using 16S rRNA gene sequencing. The nutrient-synbiotic complex presented beneficial effects against the depression-like behaviors induced by LPS, mitigated the increased level of kynurenine, and decreased levels of 5-hydroxytryptamine and BDNF both in serum and PFC (p < 0.05). It also reduced neuronal damage in PFC after LPS exposure (p < 0.05). Additionally, the nutrient-synbiotic complex effectively prevented the disturbance in abundance and diversity of the intestinal flora induced by LPS (Chao1: p = 0.013, ACE: p = 0.006, PCoA: R 2 = 0.25, p = 0.003). A total of nine bacterial genera were negatively associated with depression, while eight were positively associated with depression. Among them, g__Family_XIII_UCG_001, g__Clostridia_vadinBB60_group, and g__Lactobacillus showed significant intergroup differences (p < 0.05). This is the first study to demonstrate that a combined nutrient-synbiotic complex can prevent depressive-like behavioral changes induced by LPS. The underlying mechanisms may be associated with modifying the composition of the gut microbial community and improving the tryptophan metabolic homeostasis.
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Neuropsychological Symptoms and Intrusive Thoughts Are Associated With Worse Trajectories of Chemotherapy-Induced Nausea.
CONTEXT: Although chemotherapy-induced vomiting is well controlled with evidence-based antiemetic regimens, chemotherapy-induced nausea (CIN) remains a significant clinical problem. OBJECTIVES: Study purposes, in a sample of outpatients with breast, gastrointestinal, gynecological, or lung cancer who received two cycles of chemotherapy (CTX, n = 1251), were to evaluate for interindividual differences in the severity of CIN and to determine which demographic, clinical, symptom, and stress characteristics are associated with higher initial levels as well as with the trajectories of CIN. METHODS: Patients were recruited during their first or second cycle of CTX. Patients completed self-report questionnaires a total of six times over two cycles of CTX. Hierarchical linear modeling was used to evaluate for interindividual differences in and characteristics associated with the severity of CIN. RESULTS: Across the two cycles of CTX, higher levels of sleep disturbance, depression, and morning fatigue, as well as higher levels of intrusive thoughts, were associated with higher initial levels of CIN. In addition, lower functional status scores and shorter cycle lengths were associated with higher initial levels of CIN, and younger age and higher emetogenicity of the CTX regimen were associated with both higher initial levels as well as worse trajectories of CIN severity. CONCLUSION: These findings suggest that common symptoms associated with cancer and its treatment are associated with increased severity of CIN. Targeted interventions for these symptoms may reduce the burden of unrelieved CIN.
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Microbiome and Vocalization Biomarkers of Infant Distress, Maternal Depression and Parenting Styles.
INTRODUCTION: Psychiatric disorders have their genesis in early life. Standard screening approaches during well child visits for pathological infant distress, maternal depression, and dysfunctional parenting behaviors are likely inadequate. Microbiome measures and infant vocalizations have promise as scalable psychiatric biomarkers for infants. The purpose of this study was to examine associations among infant gut colonization based on microbiome measurements with maternal distress and maternal depressive symptoms in a sample of infants. METHODS: This study sought to examine infant microbiome correlates of infant distress, parent-infant interactions, maternal distress, and maternal depressive symptoms. We collected (N = 31) microbiome samples, infant vocalizations during vaccination, and behavioral measures during a 4 month well child visit (WCV) and did a battery of clinical assessments to assess for maternal depression, parent-child interactions, family characteristics and family stress. Whole-genome SHOTGUN sequencing was utilized to identify three types of associations: alpha-diversity using Shannon and Inverse-Simpson indexes, beta-diversity using Bray-Curtis and Jaccard distances, and differential abundance using LinDA. Spectral measures of infant cries were also modeled to assess potential relationships with clinical assessments and the microbiome. RESULTS: There were 19 phyla, 417 genera, and 1246 species identified with taxonomic classification. Maternal distress as measured by PHQ-9 scores obtained when infants were 2 months old were associated with 4 bacterial species (Actinomyces johnsonii, Bilophila wadsworthia, Clostridium dakarense and Ruminococcus flavefaciens; FDR < 0.1) and beta-diversity (p = 0.006-BC; p = 0.005-Jaccard). Infant cries with greater high frequency band power (p < 0.03) and a greater high-to-mid frequency ratio-metrics (p < 0.05) were associated with altered α-diversity of the microbiome. No correlations were present between maternal PHQ-9 at 4 months, PSI-IV and microbiome diversity. CONCLUSION: The present findings suggest that an infant stress (assessed by quality of crying) is associated with lower microbiome diversity. Decreased diversity reflects an unhealthy microbiome. Parental depressive symptoms may also influence infant microbiome. Future interventional studies focused on the quality of the infant-caregiver relationship should examine related changes in intestinal microbiota.
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Molecular mediators of the association between child obesity and mental health.
Biological mechanisms underlying the association between obesity and depression remain unclear. We investigated the role of metabolites and DNA methylation as mediators of the relationship between childhood obesity and subsequent poor mental health in the English Avon Longitudinal Study of Parents and Children. Obesity was defined according to United Kingdom Growth charts at age 7 years and mental health through the Short Mood and Feelings Questionnaire (SMFQ) completed at age 11 years. Metabolites and DNA methylation were measured by nuclear magnetic resonance spectroscopy and Illumina array in blood at the age of 7 years. The associations between obesity and SMFQ score, as continuous count data or using cut-offs to define depressive symptoms (SMFQ >7) or depression (SMFQ >11), were tested using adjusted Poisson and logistic regression. Candidate metabolite mediators were identified through metabolome-wide association scans for obesity and SMFQ score, correcting for false-discovery rate. Candidate DNA methylation mediators were identified through testing the association of putative BMI-associated CpG sites with SMFQ scores, correcting for look-up false-discovery rate. Mediation by candidate molecular markers was tested. Two-sample Mendelian randomization (MR) analyses were additionally applied to test causal associations of metabolites with depression in independent adult samples. 4,018 and 768 children were included for metabolomics and epigenetics analyses, respectively. Obesity at 7 years was associated with a 14% increase in SMFQ score (95% CI: 1.04, 1.25) and greater odds of depression (OR: 1.46 (95% CI: 0.78, 2.38) at 11 years. Natural indirect effects (mediating pathways) between obesity and depression for tyrosine, leucine and conjugated linoleic acid were 1.06 (95% CI: 1.00, 1.13, proportion mediated (PM): 15%), 1.04 (95% CI: 0.99, 1.10, PM: 9.6%) and 1.06 (95% CI: 1.00, 1.12, PM: 13.9%) respectively. In MR analysis, one unit increase in tyrosine was associated with 0.13 higher log odds of depression (p = 0.1). Methylation at cg17128312, located in the FBXW9 gene, had a natural indirect effect of 1.05 (95% CI: 1.01,1.13, PM: 27%) as a mediator of obesity and SMFQ score. Potential biologically plausible mechanisms involving these identified molecular features include neurotransmitter regulation, inflammation, and gut microbiome modulation. These results require replication in further observational and mechanistic studies.
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The Potential of Flavonoids and Flavonoid Metabolites in the Treatment of Neurodegenerative Pathology in Disorders of Cognitive Decline.
Flavonoids are a biodiverse family of dietary compounds that have antioxidant, anti-inflammatory, antiviral, and antibacterial cell protective profiles. They have received considerable attention as potential therapeutic agents in biomedicine and have been widely used in traditional complimentary medicine for generations. Such complimentary medical herbal formulations are extremely complex mixtures of many pharmacologically active compounds that provide a therapeutic outcome through a network pharmacological effects of considerable complexity. Methods are emerging to determine the active components used in complimentary medicine and their therapeutic targets and to decipher the complexities of how network pharmacology provides such therapeutic effects. The gut microbiome has important roles to play in the generation of bioactive flavonoid metabolites retaining or exceeding the antioxidative and anti-inflammatory properties of the intact flavonoid and, in some cases, new antitumor and antineurodegenerative bioactivities. Certain food items have been identified with high prebiotic profiles suggesting that neutraceutical supplementation may be beneficially employed to preserve a healthy population of bacterial symbiont species and minimize the establishment of harmful pathogenic organisms. Gut health is an important consideration effecting the overall health and wellbeing of linked organ systems. Bioconversion of dietary flavonoid components in the gut generates therapeutic metabolites that can also be transported by the vagus nerve and systemic circulation to brain cell populations to exert a beneficial effect. This is particularly important in a number of neurological disorders (autism, bipolar disorder, AD, PD) characterized by effects on moods, resulting in depression and anxiety, impaired motor function, and long-term cognitive decline. Native flavonoids have many beneficial properties in the alleviation of inflammation in tissues, however, concerns have been raised that therapeutic levels of flavonoids may not be achieved, thus allowing them to display optimal therapeutic effects. Dietary manipulation and vagal stimulation have both yielded beneficial responses in the treatment of autism spectrum disorders, depression, and anxiety, establishing the vagal nerve as a route of communication in the gut-brain axis with established roles in disease intervention. While a number of native flavonoids are beneficial in the treatment of neurological disorders and are known to penetrate the blood-brain barrier, microbiome-generated flavonoid metabolites (e.g., protocatechuic acid, urolithins, γ-valerolactones), which retain the antioxidant and anti-inflammatory potency of the native flavonoid in addition to bioactive properties that promote mitochondrial health and cerebrovascular microcapillary function, should also be considered as potential biotherapeutic agents. Studies are warranted to experimentally examine the efficacy of flavonoid metabolites directly, as they emerge as novel therapeutic options.
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Multisensory Fusion Training and 7, 8-Dihydroxyflavone Improve Amyloid-β-Induced Cognitive Impairment, Anxiety, and Depression-Like Behavior in Mice Through Multiple Mechanisms.
BACKGROUND: There is growing interest in the role of physical activity in patients with of Alzheimer's disease (AD), particularly regarding its impact of cognitive function, gut microbiota, metabolites, and neurotrophic factors. OBJECTIVE: To investigate the impact of multisensory fusion training (MSFT) combined with 7, 8-dihydroxyflavone (DHF) on the behavioral characteristics, protein expression, microbiome, and serum metabolome using the AD model in mice induced with amyloid-β (Aβ). METHODS: We assessed cognitive ability, anxiety-like and depression-like behaviors in Aβ mice using behavioral measures. Western blotting was employed to detect the expression of relevant proteins. The 16S rRNA gene sequencing and metabolomics were used to analyze changes in the intestinal microbial composition and serum metabolic profile, respectively, of Aβ mice. RESULTS: The behavioral outcomes indicated that a 4-week intervention combining DHF and MSFT yielded remarkable improvements in cognitive function and reduced anxiety and depression-like behaviors in Aβ mice. In the hippocampus of Aβ mice, the combined intervention increased the levels of BDNF, VGF, PSD-95, Nrf2, p-GSK3β and p-CREB proteins. Analyses of sequence and metabolomic data revealed that Bacteroides and Ruminococcaceae were remarkably more abundant following the combined intervention, influencing the expression of specific metabolites directly linked to the maintenance of neuronal and neurobehavioral functions. These metabolites play a crucial role in vital processes, such as amino acid metabolism, lipid metabolism, and neurotransmitter metabolism in mice. CONCLUSION: Our study highlighted that MSFT combined with DHF improves cognitive impairment, anxiety, and depression-like behavior in Aβ mice through multiple mechanisms, and further validated the correlation between the gut microbiome and serum metabolome. These findings open up a promising avenue for future investigations into potential treatment strategies for AD.
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The anti-depressive role of the Pei Yuan Kai Yu formula in cerebral small vessel disease based on gut microbiota.
BACKGROUND: Cerebral small vessel disease (CSVD), characterized by pathological changes in brain vessels, is a common cause of death in the elderly and often accompanied by depression, which significantly affects patients' quality of life and rehabilitation; understanding its pathogenesis and developing innovative therapies are urgently needed, especially considering the role of the blood - brain barrier impairment and the gut - microbiota - gut - brain axis in this complex condition. METHODS: Dahl/SS rats were fed a diet containing 8% NaCl and were subjected to chronic unpredictable mild stress (CUMS) stimulation for 4 weeks. PY (1.407 g/kg/day) was administered intragastrically to evaluate its role in CSVD with depression. Pseudo germ-free rats were colonized with gut microbiota from high-salt-fed rats exposed to CUMS, followed by PY administration. RESULTS: In rats with CSVD and depression, PY significantly increased body weight; alleviated depression-like behaviors; and decreased the levels of inflammatory cytokines such as TNF-α, IL-1β, and IL-6 in both serum and hippocampus. Additionally, PY reversed inflammation-induced nerve damage; reduced the overexpression of microglia in the hippocampus; decreased the levels of hippocampal VEGF and MMP-9, and increased the levels of hippocampal occludin, ZO-1, and claudin-5. Moreover, PY improved the composition of gut microbiota and enhanced microbial diversity. PY induced characteristic changes in the microbiome, which were associated with inflammation, endothelial dysfunction, and depressive-like behaviors. These significant metabolites were identified and were found closely related to inflammation, endothelial cell dysfunction, and depression-like behaviors. CONCLUSION: In conclusion, PY acts as an antidepressant to slow down the progression of CSVD by inhibiting microglial activation, reducing inflammation and ameliorating endothelial dysfunction. It exerts its effect, at least in part, by enhancing microbiota-mediated metabolism in vivo.
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Methodological and conceptual complexities of assessing relationships between single-occasion CRP inflammation and daily affect.
Inflammation is commonly implicated in sustained levels of depressed mood, chiefly with concurrent measures. There is a dearth of research on understanding how mood-inflammation relationships change on a day-to-day timescale. Determining how inflammation and mood may fluctuate and interact with each other is imperative to determining which pathways may lead to a depressed mood due to inflammation, and, more broadly, which factors induce inflammation in the first place. Therefore, we explored a means of elucidating the nature of mood-inflammation relationships using daily measures of mood and a single time-point measure of inflammation, C-Reactive Protein (CRP). We predicted that the relationship between affect and this measure of inflammation would be time-invariant because of evidence suggesting factors contributing to inflammation are persistent over time, such as obesity or poor gut-microbiome health. Our sample consisted of 1397 young adult participants who completed daily surveys for thirteen days and provided a blood sample for CRP measurement once at the conclusion of the study. A Bayesian multivariate regression model was performed to determine how daily levels of positive and negative mood could be predicted by this single time-point measure of inflammation. As part of our analysis, we sought to control for two key moderators, BMI and physical activity. Results indicated that moderate levels of inflammation were not associated with poor mood when the individual exercised. We also determined that high BMI participants exhibited a greater impact of inflammation on their mood relative to low BMI participants. However, contrary to our primary prediction that this mood-inflammation relationship would be time-invariant, we did indeed find that the relationship was time-variant. This result indicated that research examining associations involving inflammation daily will be required to understand which causative factors may contribute to fluctuations of a mood-inflammation relationship on a daily basis.
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Impact of Positive Glucose, Lactose, and Fructose Hydrogen Breath Tests on Symptoms and Quality of Life in Irritable Bowel Syndrome.
BACKGROUND: Gas production due to fermentation from fructose malabsorption (FM) or lactose malabsorption (LM) and small intestinal bacterial overgrowth (SIBO) contribute to the development of gastrointestinal symptoms in patients with irritable bowel syndrome (IBS). However, the impact of the carbohydrate malabsorption, unlike SIBO, is relatively unknown. METHODOLOGY: A multicenter, prospective study of consecutive adults with IBS who underwent a hydrogen breath test (HBT) (glucose, 75 g; lactose, 25 g; or fructose, 25 g) was conducted. The proportion of patients who tested positive for glucose, fructose and lactose HBT were evaluated. The symptom severity, psychology, and quality of life of subjects with SIBO were compared with those having LM and/or FM. Independent factors associated with severe IBS (IBS-symptom severity scale: IBS-SSS > 300) were explored. RESULTS: A total of 116 subjects were included (median age 56 years, male 35.3%). Of these, 23.3% (27/116), 85.7% (24/28), and 44.4% (16/36) of them tested positive for glucose, lactose, and fructose HBT, respectively. Among those with a positive HBT (n = 65), patients with SIBO were more likely to have the diarrhea-predominant subtype of IBS (77.8% vs. 47.4%, p = 0.014). Severe IBS was associated with SIBO, compared with LM/FM (SIBO: 36.4% vs. LM: 9.1%/FM 13.3%, p = 0.016). With multivariate analysis, SIBO (OR 5.25, p = 0.028) and depression (OR 5.59, p = 0.030) were independently associated with severe IBS. CONCLUSION: Although LM and FM commonly co-exist in IBS, their clinical relevance appears to be less significant than that of SIBO. The connection between SIBO with depression reinforces the importance of the microbiome-gut-brain axis in IBS.
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Decoding the gut-sleep Nexus: a bibliometric mapping of gut microbiota and sleep disorders.
BACKGROUND: An increasing number of studies have focused on the interaction between gut microbiota and sleep disorders. However, there is currently no bibliometric analysis of the literature on gut microbiota and sleep disorders. This study employs bibliometric methods to analyze the current research status and hotspots in the field of gut microbiota and sleep disorders, providing a reference for future research in this area. METHODS: Articles related to gut microbiota and sleep disorders were retrieved from the WOS core database, covering the period from the database's inception to December 31, 2024. After rigorous screening, VOSviewer and CiteSpace were used to conduct analyses on quantity, collaboration networks, clustering, and citation bursts. RESULTS: The number of articles on gut microbiota and sleep disorders has increased annually, with a significant surge after 2022. China has the highest number of publications, while the United States has the highest citation count. The institution with the most publications is Shanghai Jiao Tong University, and the institution with the most citations is Deakin University. The top 10 journals by publication volume are all ranked above Q2 in the JCR. The most cited article is "Gut microbiome diversity is associated with sleep physiology in humans" by Smith et al., published in PLOS ONE in 2019. The top 10 most frequent keywords are gut microbiota, sleep, depression, inflammation, chain fatty acids, anxiety, brain, oxidative stress, obesity, and health. The keyword cluster "obstructive sleep apnea" is a focal research direction, while fecal microbiota transplantation is a current research hotspot. CONCLUSION: This study reveals the publication trends, collaboration relationships among countries, regions, and authors, and recent research hotspots in the field of gut microbiota and sleep disorders through bibliometric methods, providing an objective data reference for scientific research in this domain.