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Optimizing intervention tools to improve nutrition and physical activity for colorectal cancer survivors (Tools To Be Fit): Study protocol of a randomized factorial experiment.
BACKGROUND: Colorectal cancer (CRC) is the 2nd leading cause of cancer death in the United States. The American Cancer Society (ACS) Nutrition and Physical Activity Guidelines are associated with longer survival among CRC survivors, but few report behaviors consistent with the guidelines. METHODS: The Tools To Be Fit study, based on the Multiphase Optimization Strategy (MOST) framework, is a full factorial experimental to optimize a remotely delivered 48-week diet and physical activity intervention for non-metastatic CRC survivors. The intervention includes a core component (booklet and personal report). CRC survivors (N = 400) are additionally randomly assigned to one of 16 combinations of four candidate components, each with 2 options: 1) text messaging (on/off); 2) self-monitoring modality (digital/paper); 3) health coaching (on/off); and 4) support person coaching (on/off). OUTCOMES: Our primary outcome is adherence to the ACS guidelines after 48 weeks using a score that includes physical activity from accelerometers, dietary intake from a food frequency questionnaire, and body mass index (BMI) measured by a technician. Secondary outcomes include the ACS score after 24 weeks and score components at 24 and 48 weeks. Exploratory outcomes include adherence and change in Social Cognitive Theory constructs. We will explore moderation by sociodemographic, clinical, and psychological/behavioral factors; and change in the ACS score in relation to change in levels of insulin, insulin sensitivity, inflammation, gut microbiome structure, fatigue, depression, and sleep disturbance. DISCUSSION: The proposed study aims to inform a randomized controlled trial to determine whether an optimized intervention reduces risk of recurrence among CRC survivors.
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The Impact of Probiotic Bacillus subtilis on Injurious Behavior in Laying Hens.
Intestinal microbiota functions such as an endocrine organ to regulate host physiological homeostasis and behavioral exhibition in stress responses via regulating the gut-brain axis in humans and other mammals. In humans, stress-induced dysbiosis of the gut microbiota leads to intestinal permeability, subsequently affecting the clinical course of neuropsychiatric disorders, increasing the frequency of aggression and related violent behaviors. Probiotics, as direct-fed microorganism, have been used as dietary supplements or functional foods to target gut microbiota (microbiome) for the prevention or therapeutic treatment of mental diseases including social stress-induced psychiatric disorders such as depression, anxiety, impulsivity, and schizophrenia. Similar function of the probiotics may present in laying hens due to the intestinal microbiota having a similar function between avian and mammals. In laying hens, some management practices such as hens reared in conventional cages or at a high stocking density may cause stress, leading to injurious behaviors such as aggressive pecking, severe feather pecking, and cannibalism, which is a critical issue facing the poultry industry due to negative effects on hen health and welfare with devastating economic consequences. We discuss the current development of using probiotic Bacillus subtilis to prevent or reduce injurious behavior in laying hens.
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An Atlas Characterizing the Shared Genetic Architecture of Inflammatory Bowel Disease with Clinical and Behavioral Traits.
BACKGROUND: Inflammatory bowel disease (IBD) development is a complex, multifactorial process that involves extrinsic and intrinsic factors such as host genetics, the immune system, the gut microbiome, and environmental risks. To help understand the genetic contribution of clinical, behavioral, psychiatric, and diet-related traits, we aim to provide a deep and comprehensive characterization of the shared genetic architecture between IBD and hundreds of potentially related traits. METHODS: Utilizing publicly available summary statistics from a previously published IBD genome-wide association study and hundreds of traits from the United Kingdom BioBank (UKBB), we performed linkage disequilibrium score regression (LDSR) analysis to estimate cross-trait genetic correlations between Crohn's disease (CD), ulcerative colitis (UC), and IBD summary statistics with the UKBB traits of interest. RESULTS: Nominally significant (P < .05) genetic correlations were observed for 181 traits in overall IBD, 239 traits in CD, and 94 traits in UC. We replicate the known association between smoking behavior and CD/UC, namely that current tobacco smoking has a positive genetic correlation with CD (rg = 0.12, P = 4.2 × 10-4), while "ever smoking" has a negative genetic correlation with UC (rg = -0.07, P = .042). Globally, all 3 strata (IBD, CD, and UC) demonstrated increased genetic correlations for psychiatric-related traits related to anxiety and depression. CONCLUSION: The present analysis reveals the shared genetic architecture between multiple traits and IBD, CD, and UC. Understanding the relevance of joint occurrences of IBD with psychiatric diseases may moderate management of these diseases for individuals jointly affected by them.
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The Microbiome and Human Biology.
Over the past few years, microbiome research has dramatically reshaped our understanding of human biology. New insights range from an enhanced understanding of how microbes mediate digestion and disease processes (e.g., in inflammatory bowel disease) to surprising associations with Parkinson's disease, autism, and depression. In this review, we describe how new generations of sequencing technology, analytical advances coupled to new software capabilities, and the integration of animal model data have led to these new discoveries. We also discuss the prospects for integrating studies of the microbiome, metabolome, and immune system, with the goal of elucidating mechanisms that govern their interactions. This systems-level understanding will change how we think about ourselves as organisms.
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Periodontitis and Neuropsychiatric Disorders: Epidemiological and Mechanistic Evidence.
This review aims to critically analyze the epidemiological evidence and mechanistic insights linking periodontitis with the onset, progression, or severity of neuropsychiatric disorders. From an epidemiological perspective, eligible evidence was identified regarding disorders related to trauma, stress, anxiety, depressive, and bipolar disorders, whereas no studies meeting the predefined inclusion criteria were found for the remaining considered disorders. The strongest epidemiological evidence was observed for depressive disorders and anxiety- and stress-related conditions. However, the predominance of cross-sectional studies, together with substantial methodological heterogeneity, limits conclusions regarding temporality and causality. From a mechanistic perspective, the available evidence regarding the association between periodontitis and neuropsychiatric disorders predominantly supports as mechanisms (1) microbial pathways (microbial translocation and functional dysregulation of the oral microbiome), (2) inflammatory and immune pathways (systemic (meta)inflammation and trafficking of immune players systemic), and (3) shared underlying vulnerabilities (behavioral factors, medication-related effects, lifestyle and systemic health factors, and genetic mechanisms). Periodontitis may promote a persistent low-grade systemic inflammatory state through the release of bacterial products and inflammatory mediators into the circulation, thereby influencing immune, neuroendocrine, and vascular pathways relevant to neuropsychiatric vulnerability. Moreover, the hematogenous dissemination or swallowing of periodontal bacteria and their virulence factors may contribute to microbial remodeling at distant sites, including the gut, supporting the concept of an oral-gut-brain axis. Overall, the evidence analyzed supports periodontitis as a potential modifiable contributor within a broader biopsychosocial network linking oral and mental health, while highlighting the need for longitudinal studies and interventional trials to clarify causality and clinical relevance.
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Association between gut microbiota and post-stroke depression in Chinese population: A meta-analysis.
BACKGROUND: Post-stroke depression (PSD) is a common neuropsychological complication after a stroke with a range of poor outcomes. Evidence of gut microbiota disorder for PSD has recently accumulated. This study aimed to systematically evaluate the association between PSD and gut microbiota. METHODS: We searched PubMed, Web of Science, Embase, and VIP, CNKI, Wangfang without language restrictions for eligible studies and performed a meta-analysis and systematic review to assess the pooled differences in gut microbiota compositions between PSD and healthy individuals. RESULTS: We included nine eligible studies reporting the differences in the intestinal microbiome between PSD and healthy control. The pooled results demonstrated that the sequencing depth index (Good's coverage), richness indexes (Chao1 and ACE), evenness, and alpha diversity (Shannon and Simpson) were not significantly changed in PSD patients as compared to healthy controls. The observed species (operational taxonomic unit, OUT) in PSD was significantly higher than that in healthy individuals (SMD, 1.86, 95%CI: 1.47 to 2.25). Furthermore, we observed significant differences between PSD and healthy individuals at the phylum level. The pooled estimation of relative abundance of Proteobacteria (SMD, 0.37, 95%CI: 0.19 to 0.55), Bacteroidetes (SMD, 1.87, 95%CI: 1.25 to 2.48), and Fusobacteria (SMD, 1.06, 95%CI: 0.76 to 1.37) in patients with PSD significantly was increased as compared to controls, while the pooled relative abundance of Firmicutes (SMD, -0.84, 95%CI: -1.21 to -0.47) was significantly decreased in PSD as compared to healthy controls. Moreover, significant differences in intestinal microbiota were observed between PSD patients and healthy controls at the family and genus levels. CONCLUSIONS: This meta-analysis indicates a significant alteration of observed species and microbiota composition at the phylum, family and genus levels in PSD as compared to healthy individuals.
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Association between Gut Microbiota and Emotional-Behavioral Symptoms in Children with Attention-Deficit/Hyperactivity Disorder.
Previous studies have explored the role of the microbiome in attention-deficit/hyperactivity disorder (ADHD). However, whether the microbiome is correlated with emotional-behavioral disturbances, the most common comorbid symptom of ADHD, remains unclear. We established a cross-sectional study in which 6- to 18-year-old children with ADHD who were receiving no medication and a healthy control group of children without ADHD were recruited to analyze their microbiome composition. Microbiota of fecal samples were collected and analyzed using a 16s rRNA gene sequencing approach. In comparison with the healthy control group, the gut microbiota in children with ADHD exhibited significantly lower beta diversity. The abundance of the phylum Proteobacteria and the genera Agathobacter, Phascolarctobacterium, Prevotella_2, Acidaminococcus, Roseburia, and Ruminococcus gnavus group was increased in the ADHD group compared with the healthy group. Linear discriminant effect size (LEfSe) analysis was used to highlight specific bacteria phylotypes that were differentially altered between the ADHD and control groups. A regression analysis was performed to investigate the association between microbiota and emotional-behavioral symptoms in children with ADHD. A significant association was noted between withdrawal and depression symptoms and Agathobacter (p = 0.044), and between rule-breaking behavior and the Ruminococcus gnavus group (p = 0.046) after adjusting for sex, age, and the ADHD core symptoms score. This study advances the knowledge of how gut microbiota composition may contribute to emotional-behavioral symptoms in children with ADHD. The detailed mechanisms underlying the role of the gut microbiota in ADHD pathophysiology still require further investigation.
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How gut microbiota contribute to neuropsychiatric disorders: evidence from neuroimaging studies.
The interaction between the gut microbiota and central nervous system (CNS) diseases has emerged as a major focus in neuroscience and microbiome research. Accumulating evidence shows that gut microbiota influence the pathogenesis of neurodevelopmental, neurodegenerative, autoimmune, and psychiatric conditions via the microbiota-gut-brain axis. However, the underlying mechanisms are complex and not yet fully elucidated. Advances in multimodal magnetic resonance imaging, positron emission tomography, and diffusion tensor imaging, now enable in vivo visualization of associations between gut microbial alterations and abnormalities in brain structure and function, providing new perspectives for understanding the role of gut microbiota in CNS pathology. This review systematically reviews neuroimaging-based research linking gut microbiota to neurological diseases (e.g., Alzheimer's disease, multiple sclerosis, traumatic brain injury), and psychiatric disorders (e.g., schizophrenia, and autism spectrum disorder). It highlights the mediating roles of microbial metabolites, immune-inflammatory responses, and neuroimmune pathways, and discusses future directions integrating multi-omics data with neuroimaging technologies, as well as their potential clinical applications. What distinguishes this review from its predecessors in the same field is its explicit neuroimaging-driven framework rather than general mechanistic discussion.
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Fecal microbiome differs between patients with systemic sclerosis with and without small intestinal bacterial overgrowth.
INTRODUCTION: Gastrointestinal manifestations of systemic sclerosis affect up to 90% of patients, with symptoms including diarrhea and constipation. Small intestinal bacterial overgrowth is a condition associated with increased numbers of pathogenic bacteria in the small bowel. While currently unknown, it has been suggested that dysregulation of the fecal microbiota may play a role in the development of systemic sclerosis and small intestinal bacterial overgrowth. OBJECTIVES: Our study aimed to describe the fecal microbiota of patients with systemic sclerosis and compare it between those with and without a diagnosis of small intestinal bacterial overgrowth. We also compared the fecal microbiota of systemic sclerosis patients with that of healthy controls to understand the association between particular bacterial taxa and clinical gastrointestinal manifestations of systemic sclerosis. METHODS: A total of 29 patients with systemic sclerosis underwent breath testing to assess for small intestinal bacterial overgrowth, provided stool samples to determine taxonomic assignments, and completed the University of California Los Angeles Scleroderma Clinical Trial Consortium Gastrointestinal Tract 2.0, which details symptoms and quality-of-life factors. Stool samples were compared between systemic sclerosis patients with and without small intestinal bacterial overgrowth, and between patients with systemic sclerosis and a healthy control cohort (n = 20), aged 18-80 years. RESULTS: Fecal microbiome analyses demonstrated differences between systemic sclerosis patients with and without small intestinal bacterial overgrowth and differences in the diversity of species between healthy controls and patients with systemic sclerosis. Trends were also observed in anticentromere antibody systemic sclerosis patients, including higher Alistipies indistincus spp. levels associated with increased methane levels of breath gas testing and higher Slakia spp. levels associated with increased rates of fecal soiling. CONCLUSIONS: Our results suggest that changes to the fecal microbiome occur in patients with small intestinal bacterial overgrowth and systemic sclerosis when compared to healthy controls. As a cross-sectional study, the potential pathophysiologic role of an altered microbiome in the development of systemic sclerosis was not considered and hence needs to be further investigated.
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Characteristics of fecal microbiota in different constipation subtypes and association with colon physiology, lifestyle factors, and psychological status.
BACKGROUND: Patients with chronic constipation (CC) show altered gut microbial composition. OBJECTIVES: To compare the fecal microbiota with different constipation subtypes and to identify potential influencing factors. DESIGN: This is a prospective cohort study. METHODS: The stool samples of 53 individuals with CC and 31 healthy individuals were analyzed using 16S rRNA sequencing. The associations between microbiota composition and colorectal physiology, lifestyle factors, and psychological distress were analyzed. RESULTS: In all, 31 patients with CC were classified as having slow-transit constipation, and 22 were classified under normal-transit constipation. The relative abundance of Bacteroidaceae was lower, and the relative abundance of Peptostreptococcaceae, Christensenellaceae, and Clostridiaceae was higher in slow-transit than in normal-transit group. In all, 28 and 25 patients with CC had dyssynergic defecation (DD) and non-DD, respectively. The relative abundance of Bacteroidaceae and Ruminococcaceae was higher in DD than in non-DD. Rectal defecation pressure was negatively correlated with the relative abundance of Prevotellaceae and Ruminococcaceae but positively correlated with that of Bifidobacteriaceae in CC patients. Multiple linear regression analysis suggested that depression was a positive predictor of Lachnospiraceae relative abundance, and sleep quality was an independent predictor of decreased relative abundance of Prevotellaceae. CONCLUSION: Patients with different CC subtypes showed different characteristics of dysbiosis. Depression and poor sleep were the main factors that affected the intestinal microbiota of patients with CC. PLAIN LANGUAGE SUMMARY: Characteristics of fecal microbiota in different constipation subtypes and association with colon physiology, lifestyle factors, and psychological status Patients with chronic constipation (CC) show altered gut microbial composition. Previous studies in CC are limited by lacking of subtype stratification, which is reflected in the lack of agreement in findings across the large number of microbiome studies. We analyzed stool microbiome of 53 CC patients and 31 healthy individuals using 16S rRNA sequencing. We found that the relative abundance of Bacteroidaceae was lower, and the relative abundance of Peptostreptococcaceae, Christensenellaceae, and Clostridiaceae was higher in slow-transit than in normal-transit CC patients. The relative abundance of Bacteroidaceae and Ruminococcaceae was higher in dyssynergic defecation (DD) than in non-DD patients with CC. In addition, depression was a positive predictor of Lachnospiraceae relative abundance, and sleep quality was an independent predictor of decreased relative abundance of Prevotellaceae in all CC patients. This study emphasizes patients with different CC subtypes have different characteristics of dysbiosis. Depression and poor sleep may be the main factors that affect the intestinal microbiota of patients with CC.