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Efficacy of double-coated probiotics for irritable bowel syndrome: a randomized double-blind controlled trial.
BACKGROUND: The purpose of this study was to elucidate the effects of a dual-coated probiotic supplement (Duolac Care) on symptoms of diarrhea-predominant irritable bowel syndrome in a randomized double-blind clinical trial. METHODS: Fifty subjects with diarrhea-predominant irritable bowel syndrome were randomly assigned to either the non-coating group or the dual-coating group in order to receive two capsules per day of multi-species probiotics containing 5 billion bacteria per capsule for 4 weeks. Data from an adequate relief questionnaire were used in assessment of primary outcome. Daily records of stool frequencies and the Bristol stool scale, a weekly symptom diary using 100-mm visual analog scale, and Beck depression inventories were collected. Blood tests including blood cell counts, interleukin-10, tumor necrosis factor-alpha and inducible nitric oxide synthase, and regulatory T cells-CD4 + CD25high T cells, CD4 + LAP + T cells and CD25high + LAP + T cells-were analyzed before and after the study. The shift of gut microbiota was investigated using a quantitative real-time polymerase chain reaction assay. RESULTS: Responses to the adequate relief questionnaire indicated significant improvement in overall discomfort in the dual-coating group and the ratio of normal stools to hard or watery stools had a better effect from dual-coated probiotics compared to non-coated probiotics. This may be due to a shift of intestinal microbiota, as our correlation analysis showed significant negative correlation between Bifidobacterium and urgency of defecation. CONCLUSIONS: Our result implies that dual-coating layers of probiotic supplement can be a candidate for treatment of diarrhea-predominant irritable bowel syndrome.
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Association between oral microbiome and depression: A population-based study.
OBJECTIVE: Depression is a global mental health issue, particularly affecting adolescents and young adults. While the role of gut microbiota in depression has been extensively studied, the influence of the oral microbiome remains underexplored. Recent studies suggest that the oral microbiome may affect systemic and brain health through the oral-brain axis. This study aimed to investigate the relationship between oral microbiome diversity and depression using data from 6212 participants in the National Health and Nutrition Examination Survey (NHANES) 2009-2012. METHODS: Oral microbiome diversity was assessed through oral rinse samples using 16S rRNA sequencing, focusing on α-diversity metrics (observed ASVs and Faith's phylogenetic diversity) and β-diversity measures. Depressive symptoms were evaluated with the Patient Health Questionnaire (PHQ-9). Weighted logistic regression models were employed to assess associations between α-diversity and depression, while linear regression was used to examine the relationship between α-diversity and PHQ-9 scores. β-diversity differences were analyzed via permutational analysis of variance (PERMANOVA). RESULTS: 10.03% of the participants were diagnosed with depression. Higher α-diversity in the oral microbiome was negatively correlated with depression: observed ASVs (OR: 0.713 [CI: 0.508-0.999], P = 0.050) and Faith's phylogenetic diversity (OR: 0.584 [CI: 0.367-0.931], P = 0.025). Linear regression indicated that greater α-diversity was associated with lower PHQ-9 scores, reflecting fewer depressive symptoms. Furthermore, β-diversity analysis revealed significant differences in the microbiome composition between depressed and non-depressed individuals. CONCLUSION: Reduced oral microbiome diversity is associated with an increased risk and severity of depression. The study underscores the importance of exploring the oral-brain axis and highlights the need for further research into the mechanisms and therapeutic strategies targeting this relationship.
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Oral Administration of 5-Hydroxytryptophan Restores Gut Microbiota Dysbiosis in a Mouse Model of Depression.
5-Hydroxytryptophan (5-HTP) has positive clinical effects on various neuropsychiatric and metabiotic disorders, especially depression. Although it increases serotonin levels in the brain and gastrointestinal tract, its pharmacology remains largely unknown. Our goal was to determine the effects of 5-HTP on the mouse gut microbiome, which has a close relationship with depression through the "microbiota-gut-brain axis." We confirmed that depressive disorder restructures the gut microbial community, and 5-HTP efficiently improves depressive symptoms in mice. Oral administration of 5-HTP significantly restored gut microbiota dysbiosis in mice with depression-like behaviors. The diversity and richness of gut microbial communities and relative abundance of specific microbial taxa at both phylum and genus levels were partially recovered. 5-HTP exhibited some positive effects on restoring the alterations in the concentrations of short-chain fatty acids and brain-derived neurotrophic factors caused by depression in mice. Our results may provide new insights into the pharmacology of 5-HTP in treating depression and other disorders.
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Investigating the Role of Gut-Derived Neurotoxin TMAO in PTSD Risk Following Traumatic Brain Injury.
BACKGROUND: Post-traumatic stress disorder (PTSD), comorbid with traumatic brain injury (TBI), severely affects the mood state of patients. Trimethylamine N-oxide (TMAO), one of the key intestinal flora metabolites, strongly correlates with TBI. This study aimed to explore the role of TMAO in the development of TBI-related PTSD and assess its predictive significance. METHODS: This study included 120 TBI patients treated at the Affiliated Hengyang Hospital of Hunan Normal University & Hengyang Central Hospital between February 2022 and April 2024. The clinical data were obtained from the hospital's medical record system. Patients were divided into a PTSD group (n = 56) and a non-PTSD group (n = 64) based on the post-traumatic stress disorder self-rating scale (PTSD-SS). Furthermore, patients in the PTSD group were divided into mild and severe subgroups. Blood samples were collected, and serum TMAO levels were assessed. Additionally, the correlation between TMAO levels, PTSD incidence, and PTSD severity was evaluated. The risk factors for PTSD comorbid with TBI and its severity were evaluated using univariate and multivariate logistic regression analyses. Finally, receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic effectiveness of TMAO as a predictive marker for PTSD. RESULTS: Multivariate analysis showed that female gender, lower per capita monthly household income, depression, anxiety, and higher serum TMAO levels were significant risk factors for PTSD. Depression, anxiety, and higher serum TMAO levels were associated with severe PTSD, and higher per capita monthly household income and intracranial infection were protective factors. Serum TMAO levels were significantly higher in PTSD patients than in non-PTSD patients (p < 0.001), with its level profoundly elevated in severe PTSD patients than in mild PTSD patients. Furthermore, the correlation analysis revealed that TMAO was positively correlated with the severity of PTSD (r = 0.8582, p < 0.0001). ROC curve analysis indicated TMAO's sensitivity of 67.86% and specificity of 93.75% for predicting PTSD, with an area under the curve (AUC) of 0.8175. CONCLUSION: Serum TMAO levels were significantly elevated in PTSD patients comorbid with TBI and were closely associated with PTSD severity. Furthermore, TMAO may aid in the early identification of high-risk, severe PTSD patients following TBI, thus helping to optimize intervention strategies.
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The effect of probiotics on anxiety, depression, nicotine dependence, and metabolic biomarkers in smokers: a randomized clinical trial.
BACKGROUND: Cigarette smoking (CS) has long been associated with both metabolic disturbances and psychological dysfunction. Recent evidence suggests that the gut microbiome may play a role in these processes. This study examined whether probiotic supplementation could influence metabolic markers, nicotine dependence, and symptoms of anxiety and depression in smokers. METHODS: In this randomized, double-blind, placebo-controlled clinical trial, seventy-four adult smokers were recruited (Kashan, Iran) and randomly assigned to receive either probiotic capsules containing Lactobacillus acidophilus, Bifidobacterium longum, Bifidobacterium bifidum, and Bifidobacterium lactis (1.8 × 10⁹ CFU/day; n = 36) or a matching placebo (n = 38) for 12 weeks. Primary endpoints included changes in depressive symptoms (Beck Depression Inventory-II; BDI-II), anxiety (Beck Anxiety Inventory; BAI), and nicotine dependence (Nicotine Dependence Syndrome Scale; NDSS). Secondary endpoints included changes in metabolic, inflammatory, and oxidative stress biomarkers. RESULTS: After 12 weeks, participants receiving probiotics showed significant reductions in fasting plasma glucose, triglycerides, very-low-density lipoprotein (VLDL) cholesterol, and C-reactive protein (CRP) compared with the placebo group (p = 0.025, p = 0.022, p = 0.026, and p = 0.004, respectively). High-density lipoprotein (HDL) cholesterol levels also increased significantly in the probiotic group (p = 0.007). No significant changes were observed in insulin, HOMA-IR, total cholesterol, LDL cholesterol, total antioxidant capacity, plasma nitric oxide, malondialdehyde, glutathione, or in scores for anxiety, depression, and nicotine dependence. CONCLUSIONS: Twelve weeks of probiotic supplementation produced favorable effects on fasting glucose, some lipid profile, and CRP levels in smokers, though no measurable benefits were observed for anxiety and depression symptoms or nicotine dependence. These findings highlight a potential metabolic benefit of probiotics in populations exposed to cigarette smoking. TRIAL REGISTRATION: This trial was registered at the Iranian Registry of Clinical Trials (IRCT20170420033551N13; registration date: December 6, 2022).
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Alpha-glycosyl isoquercitrin alleviates subchronic social defeat stress-induced depression symptoms by modulating the microbiota-gut-brain axis in mice.
AIMS: Increasing evidence suggests a link between gut microbial dysbiosis and the pathogenesis of depression. Alpha-glycosyl isoquercitrin (AGIQ), consisting of isoquercitrin and its glycosylated quercetin, has beneficial effects on the gut microbiome and brain function. Here, we detected the potential antidepressant impact of a four-week administration of AGIQ and its underlying mechanisms using a mouse model of depression. MAIN METHODS: Male C57BL/6 mice were orally administered AGIQ (0.05 % or 0.5 % in drinking water) for 28 days; subchronic social defeat stress was performed in the last 10 days. Behavior tests were conducted to assess anxiety and depressive-like behaviors. Additionally, evaluations encompassed 5-hydroxytryptamine (5-HT) levels, the gut microbiota composition, lipopolysaccharide (LPS) concentrations, short-chain fatty acids levels, and intestinal barrier integrity changes. KEY FINDINGS: AGIQ significantly alleviated depression-like behaviors and increased hippocampal 5-HT levels. Further, AGIQ mitigated stress-induced gut microbial abnormalities and reduced the levels of LPS in the serum, which affected the relative gene expression levels of 5-HT biosynthesis enzymes in vitro. Furthermore, AGIQ reversed the reduced butyrate levels in cecal contents and improved the impaired intestinal barrier by increasing the expression of colonic zonula occluden-1 (ZO-1) and occludin, thereby decreasing LPS leakage. SIGNIFICANCE: Our results suggest that AGIQ could improve stress-induced depression by regulating the gut microbiome, which inhibits LPS production and maintains the gut barrier. This is the first report on the potential effect of AGIQ on depression via the gut microbiota-brain axis, shedding new light on treatment options.
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Gut-brain axis: how the microbiome influences anxiety and depression.
Within the first few days of life, humans are colonized by commensal intestinal microbiota. Here, we review recent findings showing that microbiota are important in normal healthy brain function. We also discuss the relation between stress and microbiota, and how alterations in microbiota influence stress-related behaviors. New studies show that bacteria, including commensal, probiotic, and pathogenic bacteria, in the gastrointestinal (GI) tract can activate neural pathways and central nervous system (CNS) signaling systems. Ongoing and future animal and clinical studies aimed at understanding the microbiota-gut-brain axis may provide novel approaches for prevention and treatment of mental illness, including anxiety and depression.
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Gut-microbiome-expressed 3β-hydroxysteroid dehydrogenase degrades estradiol and is linked to depression in premenopausal females.
Estradiol decline can result in depressive disorders in females; nevertheless, the causes of this decline are unclear. In this study, we isolated estradiol-degrading Klebsiella aerogenes from the feces of premenopausal females with depression. In mice, gavaging with this strain led to estradiol decline and depression-like behaviors. The gene encoding the estradiol-degrading enzyme in K. aerogenes was identified as 3β-hydroxysteroid dehydrogenase (3β-HSD). Heterologously expressing 3β-HSD resulted in Escherichia coli obtaining the ability to degrade estradiol. Gavaging mice with 3β-HSD-expressing E. coli decreased their serum estradiol levels, causing depression-like behaviors. The prevalence of K. aerogene and 3β-HSD was higher in premenopausal women with depression than in those without depression. These results suggest that the estradiol-degrading bacteria and 3β-HSD enzymes are potential intervention targets for depression treatment in premenopausal women.
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Anxiety and small intestinal bacterial overgrowth: associations with recurrent aphthous ulcers.
BACKGROUND: Recurrent aphthous ulcer (RAU) is the most prevalent oral mucosal disease, yet its etiology remains unclear. Anxiety and depression have been linked to the onset of RAU, but research findings were contradictory. The association of intestinal diseases with RAU implies a potential role of gut microbiota in the development of this condition. This study aims to explore the correlation between the presence and severity of RAU and psychological factors, as well as gut microbiota dysbiosis. METHODS: The Zung's self-rating anxiety scale (SAS), Zung's self-rating depression scale (SDS), and Pittsburgh sleep quality index (PSQI) were used to assess the participants' psychological status. The lactulose hydrogen-methane breath test was performed to detect the presence of small intestinal bacterial overgrowth (SIBO) in RAU patients. The long-term severity of RAU is quantified using the monthly number of ulcers. Compare the differences in outcomes between individuals with RAU and the healthy population, and explore the factors influencing the severity of RAU. RESULTS: Forty-nine patients and 49 controls were included. The RAU group had significantly higher SAS scores (t = 2.18, p = 0.034), and SIBO positivity (χ2 = 75.67, p < 0.001). Factors correlated with the monthly number of ulcers included SAS score (r = 0.52, p < 0.001), symptoms of anxiety (r = 0.42, p = 0.004), SDS score (r = 0.46, p = 0.002), PSQI score (r = 0.35, p = 0.020), and SIBO positivity (r = 0.42, p = 0.005). Multiple linear regression analyses indicated that anxiety and SIBO may influence the severity of RAU. Moreover, SAS score (r = 0.38, p = 0.010) and SDS score (r = 0.38, p = 0.009) exhibited correlations with SIBO. CONCLUSIONS: RAU patients are at a higher risk of anxiety and gut microbiota dysbiosis, which could potentially escalate the severity of RAU. The role of the brain-gut axis in the pathogenesis of RAU warrants further exploration.
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[Factors supporting chronic inflammation in mental illness].
The presented literature review addresses factors and mechanisms of their influence on chronic inflammation throughout life, aggravating the severity of mental illness and contributing to its progression. Such factors include infections, intestinal microbiome disorders, lack of physical activity, overweight, chronic stress, and metabolic imbalance. Targeting these factors, in addition to standard drug therapy, can contribute to a mild course of the disease, improve the quality and duration of remissions, and, in some cases, overcome resistance to therapy.