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Dietary inflammatory index and neuropsychiatric disorders.
Neuropsychiatric disorders (NPDs) are considered a potential threat to mental health. Inflammation predominantly plays a role in the pathophysiology of NPDs. Dietary patterns are widely postulated to be involved in the physiological response to inflammation. This review aims to discuss the literature on how dietary inflammatory index (DII) is related to inflammation and, consequently, NPDs. After comprehensive scrutiny in different databases, the articles that investigated the relation of DII score and various NPDs and psychological circumstances were included. The association between dietary patterns and mental disorders comprising depression, anxiety, and stress proved the role of a proinflammatory diet in these conditions' exacerbation. Aging is another condition closely associated with DII. The impact of proinflammatory and anti-inflammatory diet on sleep quality indicated related disorders like sleep latency and day dysfunctions among the different populations are in relation with the high DII score. The potential effects of genetic backgrounds, dietary patterns, and the gut microbiome on DII are discussed as well. To plan preventive or therapeutic interventions considering the DII, these factors, especially genetic variations, should be considered as there is a growing body of literature indicating the role of personalized medicine in different NPDs. To the best of our knowledge, there is a limited number of RCTs on this subject, so future research should evaluate the causality via RCTs and look for therapeutic interventions with an eye on personalized medicine using information about DII in NPDs.
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The impact of urbanization on mood disorders: an update of recent evidence.
PURPOSE OF REVIEW: Mood disorders are highly prevalent and represent a leading cause of global disability. Urbanization holds great public health implications spanning various environmental, lifestyle behavioural, economic and social domains. Underlying risk factors for mood disorders are heterogeneous but the psychiatric literature has extended beyond individual-level risk, to account for population-level environment and social-related precursors to mental ill health. This review summarizes recent studies published since 2017 examining the impact of urbanization and associated environmental, social and lifestyle risks for mood disorders, specifically depression. RECENT FINDINGS: All identified studies examined depression or subclinical mood-related symptomatology. Recent evidence suggests individuals residing in urban areas experience increased risk of depression. Mechanistic pathways include increased exposure to noise, light and air pollution, poor quality housing, reduced diet quality, physical inactivity, economic strain and diminished social networks. The role of the gut microbiome in the development of mood disorders represents a novel research domain expected to hold potential for the psychiatric and environmental field. Further research is needed to extrapolate the relationship between increased sedentary lifestyles and technology use and depression in urban societies. SUMMARY: Recent evidence highlights the complexity and reciprocity of underlying driving factors in the relationship between urbanization and mood disorders. Future epidemiological research should continue to untangle such complexity. There was a dearth of evidence relating to urbanization and mood disorders other than depression. Future research should identify the unique experiences of vulnerable subgroups who experience disproportionate increased risk of adverse health experiences associated with urbanization.
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Global research in schizophrenia and serotonin: a bibliometric analysis.
BACKGROUND: Schizophrenia is a chronic mental illness that affects millions of individuals worldwide. The etiological origin of schizophrenia is heterogeneous, but it has been shown to be associated with dysfunction in serotonin activity, serotonin receptors, and serotonin metabolism in the brain. Bibliometric analysis is a tool used to scrutinise and analyse research activities and evidence in a specific research area. No existing bibliometric analyses have considered both serotonin and schizophrenia. METHODS: We conducted a bibliometric analysis including 12,027 studies related to the schizophrenia-serotonin link published from the inception of the study to 2023 and available in the Scopus database. We used VOSviewer software to identify global trends, analyse the author and editors keywords, the most cited articles and author, as well as the most productive institutes and journals publishing research on schizophrenia-serotonin link. RESULTS: Most publications related to the link between schizophrenia and serotonin are focused on adult humans and examine topics such as antipsychotic agents, depression, and serotonin uptake inhibitors. The Journal of Clinical Psychiatry has published the most papers on the schizophrenia-serotonin relationship. Among nations, the United States is the leader in publications. King's College London is the institution with the highest number of publications, and H. Y. Meltzer is the most influential author. Growing trends in schizophrenia-serotonin research are personalised medicine, alternative medicine, transcranial magnetic stimulation, artificial intelligence, nervous system inflammation, brain-gut axis, and the gut microbiome. CONCLUSION: Since 1950, there have been several fluctuations in the number of published studies related to schizophrenia and serotonin. We believe that the development of novel medications and treatments for schizophrenia will be increased in the future, as well as research into genetic risks, psychological factors, and cranial neuroimaging components. Future schizophrenia and serotonin research is likely to focus on personalised medicine, alternative therapies, novel pathogenesis of schizophrenia, and the use of emerging technologies such as artificial intelligence.
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Mechanisms Underlying the Anti-Depressive Effects of Regular Tea Consumption.
This article is a comprehensive review of the literature pertaining to the antidepressant effects and mechanisms of regular tea consumption. Meta-data supplemented with recent observational studies were first analyzed to assess the association between tea consumption and depression risk. The literature reported risk ratios (RR) were 0.69 with 95% confidence intervals of 0.62-0.77. Next, we thoroughly reviewed human trials, mouse models, and in vitro experiments to determine the predominant mechanisms underlying the observed linear relationship between tea consumption and reduced risk of depression. Current theories on the neurobiology of depression were utilized to map tea-mediated mechanisms of antidepressant activity onto an integrated framework of depression pathology. The major nodes within the network framework of depression included hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, inflammation, weakened monoaminergic systems, reduced neurogenesis/neuroplasticity, and poor microbiome diversity affecting the gut-brain axis. We detailed how each node has subsystems within them, including signaling pathways, specific target proteins, or transporters that interface with compounds in tea, mediating their antidepressant effects. A major pathway was found to be the ERK/CREB/BDNF signaling pathway, up-regulated by a number of compounds in tea including teasaponin, L-theanine, EGCG and combinations of tea catechins and their metabolites. Black tea theaflavins and EGCG are potent anti-inflammatory agents via down-regulation of NF-κB signaling. Multiple compounds in tea are effective modulators of dopaminergic activity and the gut-brain axis. Taken together, our findings show that constituents found in all major tea types, predominantly L-theanine, polyphenols and polyphenol metabolites, are capable of functioning through multiple pathways simultaneously to collectively reduce the risk of depression.
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A Novel Probiotic Formula, BIOCG, Protects Against Alzheimer's-Related Cognitive Deficits via Regulation of Dendritic Spine Dynamics.
BACKGROUND: The brain-gut-microbiome axis has emerged as an important pathway through which perturbations in the gut and/or microbial microenvironment can impact neurological function. Such alterations have been implicated in a variety of neuropsychiatric disorders, including depression, anxiety, and Alzheimer's Disease (AD) and the use of probiotics as therapy for these diseases remains promising. However, the mechanisms underlying the gut microenvironment's influence on disease pathogenesis and therapy remain unclear. OBJECTIVE: The objective of this study is to investigate the effect of a novel probiotic formula, BIOCG, on cognitive function and pathobiological mechanisms, including amyloid processing and dendritic spine dynamics, in a mouse model of AD. METHODS: BIOCG was administered for 3 months to 3xTg or 3xTg; Thy1-YFP AD mice and functional outcomes were assessed via behavioral testing and electrophysiology. Mechanisms relevant to AD pathogenesis including dendritic spine morphology and turnover, Amyloid Precursor Protein (APP) processing and microglial phenotype were also evaluated. Finally, we sequenced fecal samples following probiotic treatment to assess the impact on gut microbial composition and correlate the changes with the above described measures. RESULTS: Mice treated with BIOCG demonstrated preserved cognitive abilities and stronger Long- Term Potentiation (LTP), spontaneous Excitatory Postsynaptic Currents (sEPSC), and glutamate-induced LTPs, indicative of functional and electrophysiological effects. Moreover, we observed attenuated AD pathogenesis, including reduced Amyloid Beta (Aβ) burden, as well as more mature dendritic spines in the BIOCG-treated. Our finding of changes in microglial number and phenotype in the treatment group suggests that this formulation may mediate its effects via attenuation of neuroinflammation. Sequencing data confirmed that the gut microbiome in treated mice was more varied and harbored a greater proportion of "beneficial" bacteria. CONCLUSION: Overall, our results indicate that treatment with BIOCG enhances microbial diversity and, through gut-brain axis interactions, attenuates neuroinflammation to produce histologic and functional improvement in AD pathogenesis.
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Inflammatory Stress Effects on Health and Function After Spinal Cord Injury.
Background: Injury to the spinal cord produces immediate, adaptive inflammatory responses that can exacerbate the initial injury and lead to secondary damage. Thus far, researchers and clinicians have focused on modulating acute inflammation to preserve sensorimotor function. However, this singular approach risks overlooking how chronic inflammation negatively impacts the broader health of persons with a spinal cord injury (SCI). Objective: The aim of this monograph was to discuss interrelated processes causing persistent inflammatory stress after SCI, along with associated health risks. We review archetypal factors that contribute to a chronic inflammatory state, including response to injury, acute infection, and autonomic dysreflexia. Secondary complications producing and exacerbating inflammation are also discussed, including pain, depression, obesity, and injury to the integumentary and skeletal systems. Finally, we discuss the role of bacteria and the gut microbiome in this process and then conclude with a discussion on how a pro-inflammatory phenotype promotes an elevated risk for cardiovascular disease after injury. Conclusions: Effectively managing chronic inflammation should be a high priority for clinicians and researchers who seek to improve the health and life quality of persons with SCI. Chronic inflammation worsens secondary medical complications and amplifies the risk for cardiometabolic disorders after injury, directly impacting both the quality of life and mortality risk after SCI. Inflammation can worsen pain and depression and even hinder neurological recovery. It is, therefore, imperative that countermeasures to chronic inflammation are routinely considered from the point of initial injury and proceeding throughout the lifespan of the individual with SCI.
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Alteration of faecal microbiota balance related to long-term deep meditation.
BACKGROUND: Advancements in research have confirmed that gut microbiota can influence health through the microbiota-gut-brain axis. Meditation, as an inner mental exercise, can positively impact the regulation of an individual's physical and mental health. However, few studies have comprehensively investigated faecal microbiota following long-term (several years) deep meditation. Therefore, we propose that long-term meditation may regulate gut microbiota homeostasis and, in turn, affect physical and mental health. AIMS: To investigate the effects of long-term deep meditation on the gut microbiome structure. METHODS: To examine the intestinal flora, 16S rRNA gene sequencing was performed on faecal samples of 56 Tibetan Buddhist monks and neighbouring residents. Based on the sequencing data, linear discriminant analysis effect size (LEfSe) was employed to identify differential intestinal microbial communities between the two groups. Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) analysis was used to predict the function of faecal microbiota. In addition, we evaluated biochemical indices in the plasma. RESULTS: The α-diversity indices of the meditation and control groups differed significantly. At the genus level, Prevotella and Bacteroides were significantly enriched in the meditation group. According to the LEfSe analysis, two beneficial bacterial genera (Megamonas and Faecalibacterium) were significantly enriched in the meditation group. Functional predictive analysis further showed that several pathways-including glycan biosynthesis, metabolism and lipopolysaccharide biosynthesis-were significantly enriched in the meditation group. Moreover, plasma levels of clinical risk factors were significantly decreased in the meditation group, including total cholesterol and apolipoprotein B. CONCLUSIONS: Long-term traditional Tibetan Buddhist meditation may positively impact physical and mental health. We confirmed that the gut microbiota composition differed between the monks and control subjects. The microbiota enriched in monks was associated with a reduced risk of anxiety, depression and cardiovascular disease and could enhance immune function. Overall, these results suggest that meditation plays a positive role in psychosomatic conditions and well-being.
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Epigenetic Alterations of Brain Non-Neuronal Cells in Major Mental Diseases.
The tissue-specific expression and epigenetic dysregulation of many genes in cells derived from the postmortem brains of patients have been reported to provide a fundamental biological framework for major mental diseases such as autism, schizophrenia, bipolar disorder, and major depression. However, until recently, the impact of non-neuronal brain cells, which arises due to cell-type-specific alterations, has not been adequately scrutinized; this is because of the absence of techniques that directly evaluate their functionality. With the emergence of single-cell technologies, such as RNA sequencing (RNA-seq) and other novel techniques, various studies have now started to uncover the cell-type-specific expression and DNA methylation regulation of many genes (e.g., TREM2, MECP2, SLC1A2, TGFB2, NTRK2, S100B, KCNJ10, and HMGB1, and several complement genes such as C1q, C3, C3R, and C4) in the non-neuronal brain cells involved in the pathogenesis of mental diseases. Additionally, several lines of experimental evidence indicate that inflammation and inflammation-induced oxidative stress, as well as many insidious/latent infectious elements including the gut microbiome, alter the expression status and the epigenetic landscapes of brain non-neuronal cells. Here, we present supporting evidence highlighting the importance of the contribution of the brain's non-neuronal cells (in particular, microglia and different types of astrocytes) in the pathogenesis of mental diseases. Furthermore, we also address the potential impacts of the gut microbiome in the dysfunction of enteric and brain glia, as well as astrocytes, which, in turn, may affect neuronal functions in mental disorders. Finally, we present evidence that supports that microbiota transplantations from the affected individuals or mice provoke the corresponding disease-like behavior in the recipient mice, while specific bacterial species may have beneficial effects.
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Safety and Efficacy of Ketogenic Diet in the Management of Multiple Sclerosis: A Systematic Review.
This systematic review examines the safety and efficacy of ketogenic diets (KD) in multiple sclerosis (MS) management. Following Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines, we systematically searched five major databases through April 2025, identifying six relevant studies published between 2017 and 2024. These studies, predominantly focusing on relapsing-remitting MS, demonstrate consistent benefits of ketogenic interventions across multiple domains. Findings suggest KD normalizes gut microbiome composition, reduces pro-inflammatory markers (ALOX5, COX1, COX2), improves body composition with favorable changes in adipokines (decreased leptin, increased adiponectin), and enhances clinical outcomes, including fatigue, depression, sleep quality, and quality of life measures. Objective neurological improvements were observed in Expanded Disability Status Scale (EDSS) scores, walking ability, and manual dexterity. Adherence rates were notably high, with benefits partially persisting after intervention completion. The metabolic shift induced by ketosis may provide alternative neuronal energy substrates, reduce oxidative stress, and attenuate neuroinflammation. Despite limitations including small sample sizes and study heterogeneity, these preliminary findings suggest KDs represent a promising adjunctive approach in MS management, addressing both inflammatory and neurodegenerative components of the disease. Larger, controlled trials with longer follow-up periods are warranted to establish long-term safety and efficacy profiles.
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Efficacy of prebiotics, probiotics, and postbiotics on depression: a systematic review and meta-analysis of randomized controlled trials.
BACKGROUND: Depression is a global health issue linked to gut-microbiota-dysbiosis, which influences brain function through the gut-brain axis. Dietary biotics offer a promising therapeutic avenue. OBJECTIVE: This systematic review and meta-analysis aimed to evaluate the efficacy of biotic interventions in managing depression. METHODOLOGY: Five databases were searched for randomized controlled trials (RCTs) from 2016 to 2024. 27 RCTs with a control group and standard depression rating scales were included. Data extraction and risk-of-bias assessment were conducted independently by two reviewers, with certainty-of-evidence appraised using GRADE. Meta-analyses employed standardized mean differences, with subgroup analyses by intervention duration (short: <6 weeks, medium: 6-12 weeks, and long: >12 weeks), respectively. RESULTS: Probiotic interventions showed no significant effects in short and medium-duration subgroups (6 and 12 studies, respectively), both of which demonstrated substantial heterogeneity. A significant effect was observed in the long-duration subgroup (2 studies) with no observed heterogeneity, although based on limited evidence. Prebiotic interventions showed no significant effects, while postbiotic interventions demonstrated no clear effects across durations, with variable heterogeneity. Sensitivity analyses were generally consistent with the main findings. Overall certainty of evidence was rated as moderate due to inconsistency across studies. CONCLUSION: Probiotics administered over longer durations may be associated with improvements in depressive symptoms, although this finding is based on limited evidence. Evidence for prebiotic and postbiotic interventions remains inconclusive. Overall, substantial heterogeneity was observed across studies, and findings should be interpreted cautiously. Further well-designed randomized controlled trials are needed to clarify the effects of microbiome-targeted interventions in depression.