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Abundance of Probiotics and Butyrate-Production Microbiome Manages Constipation via Short-Chain Fatty Acids Production and Hormones Secretion.
SCOPE: The characteristics of gut microbiota and host metabolism are hypothesized to be associated with constipation status, but the regulation mechanism is not fully understood. Thus, the current study investigates the effect of constipation symptoms on gut functionality following the modulation of gut microbiota and metabolites via dietary fiber intervention. METHODS AND RESULTS: Constipation causes a significantly reduced short-chain fatty acids (SCFAs) production and a higher level of iso-butyrate. The feces of constipated people are characterized with inhibited Faecalibacterium, Ruminococcaceae and Roseburia abundance. Desulfovibrionaceae is identified to be an important endotoxin producer in constipated patients, and a butyrate-enriched SCFAs profile achieved by dietary fiber supplement accelerates gastrointestinal transit and increases the thickness of the mucosal layer, possibly through triggering the secretion of colonic hormones and enhancing the expression of tight junction proteins for maintaining intestinal barrier integrity. More importantly, an interacting regulatory mechanism among SCFAs, in particular butyrate and propionate, may be involved in signaling between the microbiome and host cells in the colon. CONCLUSION: Gut microbiota, characterized with enriched butyrate-producing and depressed Desulfovibrionaceae bacteria, attenuates constipation symptoms through promoting intestinal hormones secretion and maintaining gut barrier integrity.
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Home-based exercise training influences gut bacterial levels in multiple sclerosis.
BACKGROUND: Multiple sclerosis is associated with gut microbiome alterations. The current study aimed to investigate the effect of home-based exercise on gut bacteria in people with multiple sclerosis (MS). We also examined the association of exercise-induced gut bacterial modulation with circulating levels of inflammatory and anti-inflammatory cytokines. MATERIALS AND METHODS: Forty-two people with MS (female/male: 31/11, expanded disability scale status <5) participated in this study and were divided into two groups: 6 months of home-based exercise (5 sessions per week) and controls. Before and after the intervention, the following parameters were assessed: gut microbiota, including faecalibacterium prausnitzii, akkermansia muciniphila, prevotella and bacteroides counts; cytokine levels including interleukin (IL)-10 and tumor necrosis factor-alpha (TNF-α); and psychosocial factors including anxiety, depression, and fatigue. RESULTS: Home-based exercise significantly increased prevotella counts, and decreased akkermansia muciniphila counts (p < 0.05); however, there were no significant effects on faecalibacterium prausnitzii and bacteroides counts (p > 0.05). There were no significant effects of home-based exercise on circulating cytokine levels (p > 0.05). Moreover, home-based exercise was associated with significant improvements in anxiety and depression (p < 0.05); however, fatigue revealed no significant change (p > 0.05). Akkermansia muciniphila, prevotella and bacteroides count changes in response to the intervention were correlated with changes in IL-10 (r = -0.052, r = 0.67, and r = -0.55, respectively). CONCLUSION: In general, our data revealed the effect of exercise on gut bacteria, especially prevotella, and akkermansia muciniphila counts, which can probably have a beneficial effect on MS disease pathology and course; however, the lack of changes in cytokines following exercise suggests the possible role of mechanisms other than modulation of circulating IL-10 and TNF- α levels.
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The critical role of gut-brain axis microbiome in mental disorders.
The Gut-brain axis is a bidirectional neural and humoral signaling that plays an important role in mental disorders and intestinal health and connects them as well. Over the past decades, the gut microbiota has been explored as an important part of the gastrointestinal tract that plays a crucial role in the regulation of most functions of various human organs. The evidence shows several mediators such as short-chain fatty acids, peptides, and neurotransmitters that are produced by the gut may affect the brain's function directly or indirectly. Thus, dysregulation in this microbiome community can give rise to several diseases such as Parkinson's disease, depression, irritable bowel syndrome, and Alzheimer's disease. So, the interactions between the gut and the brain are significantly considered, and also it provides a prominent subject to investigate the causes of some diseases. In this article, we reviewed and focused on the role of the largest and most repetitive bacterial community and their relevance with some diseases that they have mentioned previously.
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The oropharyngeal microbiome is altered in individuals with schizophrenia and mania.
It is being increasingly recognized that human mucosal surfaces are not sterile but are colonized with microorganisms collectively known as the microbiome. The microbiome can alter brain functioning in humans and animals by way of a series of interactions operative in the brain-immune-gut interactome. We characterized the oropharyngeal microbiome in 316 individuals, including 121 with schizophrenia, 62 with mania, 48 with major depressive disorder, and 85 controls without a psychiatric disorder. We found that the oropharyngeal microflora of individuals with schizophrenia and individuals with mania differed from controls in composition and abundance as measured by the weighted UniFrac distance (both p < .003 adjusted for covariates and multiple comparisons). This measure in individuals with major depressive disorder did not differ from that of controls. We also identified five bacterial taxa which differed among the diagnostic groups. Three of the taxa, Neisseria subflava, Weeksellaceae, and Prevotella, were decreased in individuals with schizophrenia or mania as compared to controls, while Streptococci was increased in these groups. One taxa, Schlegelella, was only found in individuals with mania. Neisseria subflava was also positively associated with cognitive functioning as measured by the Repeatable Battery for the Assessment of Neuropsychological Status. There were no taxa significantly altered in individuals with major depression. Individuals with schizophrenia and mania have altered compositions of the oropharyngeal microbiome. An understanding of the biology of the microbiome and its effect on the brain might lead to new insights into the pathogenesis, and ultimately, the prevention and treatment of these disorders.
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Gut microbiota links to cognitive impairment in bipolar disorder via modulating synaptic plasticity.
BACKGROUND: Cognitive impairment is an intractable clinical manifestation of bipolar disorder (BD), but its underlying mechanisms remain largely unexplored. Preliminary evidence suggests that gut microbiota can potentially influence cognitive function by modulating synaptic plasticity. Herein, we characterized the gut microbial structure in BD patients with and without cognitive impairment and explored its influence on neuroplasticity in mice. METHODS: The gut structure of microbiota in BD without cognitive impairment (BD-nCI) patients, BD with cognitive impairment (BD-CI) patients, and healthy controls (HCs) were characterized, and the correlation between specific bacterial genera and clinical parameters was determined. ABX-treated C57 BL/J male mice were transplanted with fecal microbiota from BD-nCI, BD-CI patients or HCs and subjected to behavioral testing. The change of gut microbiota in recipient mice and its influence on the dendritic complexity and synaptic plasticity of prefrontal neurons were examined. Finally, microbiota supplementation from healthy individuals in the BD-CI mice was performed to further determine the role of gut microbiota. RESULTS: 16S-ribosomal RNA gene sequencing reveals that gut microbial diversity and composition are significantly different among BD-nCI patients, BD-CI patients, and HCs. The Spearman correlation analysis suggested that glucose metabolism-related bacteria, such as Prevotella, Faecalibacterium, and Roseburia, were correlated with cognitive impairment test scores, and inflammation-related bacteria, such as Lachnoclostridium and Bacteroides, were correlated with depressive severity. Fecal microbiota transplantation resulted in depression-like behavior, impaired working memory and object recognition memory in BD-CI recipient mice. Compared with BD-nCI mice, BD-CI mice exhibited more severely impaired object recognition memory, along with greater reductions in dendritic complexity and synaptic plasticity. Supplementation of gut microbiota from healthy individuals partially reversed emotional and cognitive phenotypes and neuronal plasticity in BD-CI mice. CONCLUSIONS: This study first characterized the gut microbiota in BD-CI patients and highlighted the potential role of gut microbiota in BD-related cognitive deficits by modulating neuronal plasticity in mice model.
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Probiotics and pregabalin combination prevented ictogenesis, neurobehavioral abnormalities and neurodegeneration in pentylenetetrazole kindling model of epilepsy.
The microbiota-gut-brain axis (MGBA) has emerged as a critical frontier in understanding neurological disorders, including epilepsy. Microbial disequilibrium potentially alters brain homeostasis and could potentiate an inflammatory state linking intestinal dysbiosis and intractable seizures. The current study sought to probe the anti-kindling, electrographical, behavioral and neuropathological impacts of combined intervention of probiotics (PRO; 10 ml/kg) and pregabalin (PRG; 10 mg/kg) in PTZ-induced epileptic mice for 21 days. Adult BALB/c mice were kindled via subthreshold dose of (PTZ 40 mg/kg) until mice reached seizure stage of 4-5. After the procedure, mice were tested using a set of behavioral tests, and redox alterations along with cellular pathology were assessed. vEEG monitoring revealed that kindling instigated recurrent polyspikes of high amplitude with generalized epileptic seizures which were markedly impeded in the mice treated with dual regime suggesting potential preventive impact of probiotic therapy on neuronal hyperexcitability. Additionally, combination intervention exerted positive behavioral outcomes as it ameliorated anxiety and depressive-like phenotypes along with cognitive impairments (P < 0.05) vs. PTZ control. Moreover, probiotic and pregabalin therapy incurred gut-microbiota antioxidant neuroprotection and prevented morbid neurodegeneration as evidenced by decreased production of oxidative stressors (MDA and AchE; p < 0.01) and increase in activity of antioxidant factors (SOD; P < 0.01 and CAT; P < 0.05). Furthermore, these commensal species and PRG duo regulates inflammation and halted neuronal apoptosis in CA1 and CA3 subfields of the cornu-ammonis. Overall, our findings support probiotics as an adjuvant therapy to shift treatment paradigms in drug-resistant epilepsy by altering gut-microbiome pathological neural links.
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Altered Composition of Gut Microbiota in Depression: A Systematic Review.
Cumulative evidence shows a linkage between gut microbiota pattern and depression through the brain-gut microbiome axis. The aim of this systematic review was to identify the alterations of the gut microbiota patterns in people with depression compared to healthy controls. A comprehensive literature search of human studies, published between January 2000 and June 2019, was reviewed. The key words included gastrointestinal microbiome, gut microbiome, microbiota, depression, depressive symptoms, and depressive disorder. The systematic review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. Nine articles met the eligibility criteria. Disparities in α-diversity and β-diversity of the microbiota existed in people with depression compared to healthy controls. At the phylum level, there were inconsistencies in the abundance of Firmicutes, Bacteroidetes, and Proteobacteria. However, high abundance in Actinobacteria and Fusobacteria phyla were observed in people with depression. On the family level, high abundance of Actinomycineae, Coriobacterineae, Bifidobacteriaceae, Clostridiales incertae sedis XI, Porphyromonadaceae, Clostridiaceae, Lactobacillaceae, Streptococcaceae, Eubacteriaceae, Thermoanaerobacteriaceae, Fusobacteriaceae, Nocardiaceae, Streptomycetaceae, and low abundance of Veillonellaceae, Prevotellaceae, Bacteroidaceae, Sutterellaceae, Oscillospiraceae, Marniabilaceae, and Chitinophagaceae were observed in people with depression. On the genus level, high abundance of Oscillibacter, Blautia, Holdemania, Clostridium XIX, Anaerostipes, Anaerofilum, Streptococcus, Gelria, Turicibacter, Parabacteroides, Eggerthella, Klebsiella, Paraprevotella, Veillonella, Clostridium IV, Erysipelotrichaceae incertae sedis, Eubacterium, Parvimonas, Desulfovibrio, Parasutterella, Actinomyces, Asaccharobacter, Atopobium, Olsenella and low abundance of Coprococcus, Lactobacillus, Escherichia/Shigella, Clostridium XlVa, Dialister, Howardella, Pyramidobacter, and Sutterella were found in people with depression. Alteration of gut microbiome patterns was evident in people with depression. Further evidence is warranted to allow for the translation of microbiome findings toward innovative clinical strategies that may improve treatment outcomes in people with depression.
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Ketamine interactions with gut-microbiota in rats: relevance to its antidepressant and anti-inflammatory properties.
BACKGROUND: Appreciable evidence suggest that dysbiosis in microbiota, reflected in gut microbial imbalance plays a key role in the pathogenesis of neuropsychiatric disorders including depression and inflammatory diseases. Recently, the antidepressant properties of ketamine have gained prominence due to its fast and long lasting effects. Additional uses for ketamine in inflammatory disorders such as irritable bowel syndrome have been suggested. However, ketamine's exact mechanism of action and potential effects on microbiome is not known. Here, we examined the effects of low dose ketamine, known to induce antidepressant effects, on stool microbiome profile in adult male Wistar rats. Animals (5/group) were injected intraperitoneally with ketamine (2.5 mg/kg) or saline, daily for 7 days and sacrificed on day 8 when intestinal stools were collected and stored at - 80 °C. DNA was extracted from the samples and the 16 S rRNA gene-based microbiota analysis was performed using 16S Metagenomics application. RESULTS: At genus-level, ketamine strikingly amplified Lactobacillus, Turicibacter and Sarcina by 3.3, 26 and 42 fold, respectively. Conversely, opportunistic pathogens Mucispirillum and Ruminococcus were reduced by approximately 2.6 and 26 fold, respectively, in ketamine group. Low levels of Lactobacillus and Turicibacter are associated with various disorders including depression and administration of certain species of Lactobacillus ameliorates depressive-like behavior in animal models. Hence, some of the antidepressant effects of ketamine might be mediated through its interaction with these gut bacteria. Additionally, high level of Ruminococcus is positively associated with the severity of irritable bowel syndrome (IBS), and some species of Mucispirillum have been associated with intestinal inflammation. Indirect evidence of anti-inflammatory role of Sarcina has been documented. Hence, some of the anti-inflammatory effects of ketamine and its usefulness in specific inflammatory diseases including IBS may be mediated through its interaction with these latter bacteria. CONCLUSION: Our data suggest that at least some of the antidepressant and anti-inflammatory effects of daily ketamine treatment for 7 days may be mediated via its interaction with specific gut bacteria. These findings further validate the usefulness of microbiome as a target for therapeutic intervention and call for more detailed investigation of microbiome interaction with central mediators of mood and/or inflammatory disorders.
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Hypoglycemic activity of the Baker's yeast β-glucan in obese/type 2 diabetic mice and the underlying mechanism.
SCOPE: β-Glucans have been shown to reduce the risk of obesity and diabetes. However, they often contain diverse polysaccharides and other ingredients, leading to elusive experimental data and mechanisms. In this study, a pure β-glucan was obtained from the crude Baker's yeast polysaccharides for investigating its effect on the metabolic disorders in high-fat diet induced obese (DIO)/type 2 diabetic (T2D) mice and the underlying mechanism. METHODS AND RESULTS: The Fourier transform infrared spectroscopy and nuclear magnetic resonance spectroscopy data indicated that the pure β-glucan (BYGlc) was a linear β-(1→3)-glucan. It was first found that the oral administration of BYGlc into T2D and DIO mice significantly downregulated the blood glucose through suppressing sodium-glucose transporter-1 expression in intestinal mucosa. Meanwhile, BYGlc promoted glycogen synthesis and inhibited fat accumulation in liver, and depressed macrophage infiltration and pro-inflammatory cytokines production measured by histochemistry/immunohistochemistry and ELISA. Additionally, BYGlc remarkably decreased Firmicutes population and increased the proportion of Akkermansia by 16S rDNA analysis. CONCLUSION: BYGlc showed hypoglycemic activity accompanied by promotion of metabolism and inhibition of inflammation in T2D/DIO mice model. The hypoglycemic mechanisms were first declared to be through suppressing sodium-glucose transporter-1 expression and possibly associated with the altered gut microbiota.
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Convergence of Two Fields-Breastfeeding and Lifestyle Medicine: Integrating Early Nutrition and Wellness for Lifelong Outcomes: A Tribute to Dr. Ruth Lawrence, A Pioneer in Both Fields.
Breastfeeding medicine and lifestyle medicine are grounded in preventive health and holistic care, emphasizing early interventions that foster long-term wellness. Dr. Ruth Lawrence, a pioneer in breastfeeding medicine, recognized breastfeeding as a cornerstone of preventive care, advocating for its profound impact on maternal and infant health. Her seminal work, Breastfeeding: A Guide for the Medical Profession, and her role in founding the journal Breastfeeding Medicine have been instrumental in shaping the field, emphasizing both the nutritional and psychosocial benefits of breastfeeding. Breastfeeding provides optimal nutrition, immune protection, and metabolic programming, reducing the risk of acute infections, chronic diseases, and maternal conditions such as postpartum depression and cancer. Similarly, lifestyle medicine focuses on modifiable factors-nutrition, physical activity, stress management, and sleep hygiene-to improve lifelong health outcomes. These fields converge in their shared emphasis, for example, on the gut microbiome, a critical determinant of immune and metabolic health. Breastfed infants have more diverse and beneficial gut microbiota, which reduce the risk of obesity and metabolic disorders, a focus paralleled by lifestyle medicine's advocacy for plant-based, fiber-rich diets. This review explores the parallels between breastfeeding and lifestyle medicine, advocating for research that moves beyond isolated nutrient analysis to examining whole dietary patterns in breastfeeding mothers. Maternal diet during lactation enhances the bioactive components of breast milk, including prebiotics, probiotics, and immune factors, amplifying its preventive effects. By integrating Dr. Lawrence's forward-thinking principles with insights from lifestyle medicine, breastfeeding medicine can advance its understanding of how maternal nutrition and modifiable lifestyle factors optimize health outcomes for both mother and infant, underscoring the transformative potential of early interventions in shaping lifelong health.