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Microbiome and genetic predictors of weight loss 12 months postsleeve gastrectomy: insights from a pilot retrospective cohort study.
BACKGROUND: Gut microbiome and genetic biomarkers are increasingly guiding obesity treatment. Bariatric surgery leads to shifts in gut microbial composition and function, while genome-wide association studies reveal genetic underpinnings of polygenic obesity, informing risk, therapeutic outcomes, and nutrigenomics-based interventions. OBJECTIVES: This pilot study aimed to identify gut microbiome and genetic biomarkers associated with weight loss 12 months after sleeve gastrectomy (SG). SETTING: Single academic institution university clinic. METHODS: Sixty-seven patients 12 months post-SG were enrolled: 34 had successful excess weight loss (EWL ≥50%), while 33 had unsuccessful EWL (EWL <50%). Microbiome and genetic profiles were collected and analyzed using ANOVA and regression methods. RESULTS: The genus Akkermansia was significantly associated with EWL (P = 9.9 × 10-6). Several microbial pathways, including propionate synthesis and menaquinone (vitamin K2) production, showed nominally significant (P < .05) associations with greater weight loss. No differences emerged in the Firmicutes/Bacteroidetes ratio. Genetic analyses revealed significant correlations between EWL and polygenic scores for dietary needs and metabolic responses, including distinct vitamin D and K requirements, as well as higher LDL cholesterol levels and predisposition for major depression. CONCLUSIONS: These findings suggest that both the gut microbiome and genetics may modulate weight loss following bariatric surgery. Integrating microbiome and genetic profiling into bariatric care pathways could enhance personalized obesity treatment. While this pilot, exploratory, and proof-of-concept study has limitations, it supports prior work linking gut microbial pathways to weight loss and suggests new associations. Follow-up studies are warranted to validate these results and further inform precision obesity interventions.
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The Co-Metabolism within the Gut-Brain Metabolic Interaction: Potential Targets for Drug Treatment and Design.
We know that within the complex mammalian gut is any number of metabolic biomes. The gut has been sometimes called the "second brain" within the "gut-brain axis". A more informative term would be the gut-brain metabolic interactome, which is coined here to underscore the relationship between the digestive system and cognitive function or dysfunction as the case may be. Co-metabolism between the host and the intestinal microbiota is essential for life's processes. How diet, lifestyle, antibiotics and other factors shape the gut microbiome constitutes a rapidly growing area of research. Conversely, the gut microbiome also affects mammalian systems. Metabolites of the gut-brain axis are potential targets for treatment and drug design since the interaction or biochemical interplay results in net metabolite production or end-products with either positive or negative effects on human health. This review explores the gut-brain metabolic interactome, with particular emphasis on drug design and treatment strategies and how commensal bacteria or their disruption lead to dysbiosis and the effect this has on neurochemistry. Increasing data indicate that the intestinal microbiome can affect neurobiology, from mental and even behavioral health to memory, depression, mood, anxiety, obesity, cravings and even the creation and maintenance of the blood brain barrier.
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The role of the Mediterranean diet in modulating the gut microbiome: A review of current evidence.
The Mediterranean diet (MedDiet) is recognized as one of the United Nations Educational, Scientific and Cultural Organization Intangible Cultural Heritage assets associated with lower rates of cardiometabolic diseases; lower prevalence of cancer, Alzheimer's disease, depression, and onset of inflammatory bowel disease; and more generally low-grade inflammation and mortality risks. Beyond being an input source of beneficial micronutrients, it recently has been discovered that the MedDiet plays a role in a more complex human microbiome-mediated mechanism. An interesting hypothesis suggests a bidirectional relationship between the MedDiet and the gut microbiome, where gut microbiota assembly and biosynthetic capacity are responsive to the diet; in return, the microbiome-reachable nutrients shape and modulate the microbiome toward a characteristic probiotic state. It can be speculated that that primary health benefits of the MedDiet exerted via the gut microbiome are mediated by the bioactive compounds transformed by the microbiome. Furthermore, it is possible that additional probiotic properties of the organisms promoted by diet adherence have secondary benefits. As more detailed omic-based studies take place, more evidence on the MedDiet as a core generic probiotic microbiome modulation strategy surface. However, individual-specific microbiome compositions might impose personal variations on the diet outcome. Therefore, a prospective strategy of a fine-tuned precision nutrition approach might deliver optimized benefits of the MedDiet.
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Serotonin: A mediator of the gut-brain axis in multiple sclerosis.
BACKGROUND: The significance of the gut microbiome for the pathogenesis of multiple sclerosis (MS) has been established, although the underlying signaling mechanisms of this interaction have not been sufficiently explored. OBJECTIVES: We address this point and use serotonin (5-hydroxytryptamine (5-HT))-a microbial-modulated neurotransmitter (NT) as a showcase to demonstrate that NTs regulated by the gut microbiome are potent candidates for mediators of the gut-brain axis in demyelinating disorders. Methods, Results, and Conclusion: Our comprehensive overview of literature provides evidence that 5-HT levels in the gut are controlled by the microbiome, both via secretion and through regulation of metabolites. In addition, we demonstrate that the gut microbiome can influence the formation of the serotonergic system (SS) in the brain. We also show that SS alterations have been related to MS directly-altered expression of 5-HT transporters in central nervous system (CNS) and indirectly-beneficial effects of 5-HT modulating drugs on the course of the disease and higher prevalence of depression in patients with MS. Finally, we discuss briefly the role of other microbiome-modulated NTs such as γ-aminobutyric acid and dopamine in MS to highlight a new direction for future research aiming to relate microbiome-regulated NTs to demyelinating disorders.
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Nanocellulose dysregulated glucose homeostasis in female mice on a Western diet: The role of gut microbiome.
There is currently increased interest in nanocellulose as a food emulsifier and dietary supplement. It was hypothesized that nanocellulose could modulate behaviors and glucose homeostasis in female mice using mechanisms of altered gut microbiome and immune modulation. An initial experiment was conducted with the objective of examining whether three common types of nanocellulose affected the gut microbiome of female C57BL/6 mice on a Western diet. Cellulose nanofibrils (CNF), TEMPO-CNF and cellulose nanocrystals were administered at the physiologically relevant dose of 30 mg/kg/day for 30 days by gavage, with cellulose and water groups as the positive and negative controls, respectively. Findings suggested that CNF had the strongest effect on the gut microbiome. CNF was therefore selected for a chronic 6-month study on the gut microbiome, immune system and behaviors in female NOD mice, a model for type 1 diabetes. Gut microbiome analysis suggested that there might be some beneficial changes following subchronic exposure (e.g., at the two-month timepoint), however, this effect was no longer seen after chronic consumption (e.g., at the six-month timepoint). CNF treatment also altered the immune homeostasis, including decreases in the splenic Mac-3+ population and serum level of proinflammatory chemokine LIX. Additionally, CNF consumption decreased diabetic incidences but had no effect on the depressive-like behavior and grip strength. However, further analysis, e.g., the insulin tolerance test, indicated that CNF-treated NOD mice might exhibit signs of insulin resistance. Taken together, nanocellulose dysregulated glucose homeostasis in female mice on a Western diet involving mechanisms related to alteration of the gut microbiome.
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Perturbations in Gut Microbiota Composition in Psychiatric Disorders: A Review and Meta-analysis.
IMPORTANCE: Evidence of gut microbiota perturbations has accumulated for multiple psychiatric disorders, with microbiota signatures proposed as potential biomarkers. However, no attempts have been made to evaluate the specificity of these across the range of psychiatric conditions. OBJECTIVE: To conduct an umbrella and updated meta-analysis of gut microbiota alterations in general adult psychiatric populations and perform a within- and between-diagnostic comparison. DATA SOURCES: Cochrane Library, PubMed, PsycINFO, and Embase were searched up to February 2, 2021, for systematic reviews, meta-analyses, and original evidence. STUDY SELECTION: A total of 59 case-control studies evaluating diversity or abundance of gut microbes in adult populations with major depressive disorder, bipolar disorder, psychosis and schizophrenia, anorexia nervosa, anxiety, obsessive compulsive disorder, posttraumatic stress disorder, or attention-deficit/hyperactivity disorder were included. DATA EXTRACTION AND SYNTHESIS: Between-group comparisons of relative abundance of gut microbes and beta diversity indices were extracted and summarized qualitatively. Random-effects meta-analyses on standardized mean difference (SMD) were performed for alpha diversity indices. MAIN OUTCOMES AND MEASURES: Alpha and beta diversity and relative abundance of gut microbes. RESULTS: A total of 34 studies provided data and were included in alpha diversity meta-analyses (n = 1519 patients, n = 1429 control participants). Significant decrease in microbial richness in patients compared with control participants were found (observed species SMD = -0.26; 95% CI, -0.47 to -0.06; Chao1 SMD = -0.5; 95% CI, -0.79 to -0.21); however, this was consistently decreased only in bipolar disorder when individual diagnoses were examined. There was a small decrease in phylogenetic diversity (SMD = -0.24; 95% CI, -0.47 to -0.001) and no significant differences in Shannon and Simpson indices. Differences in beta diversity were consistently observed only for major depressive disorder and psychosis and schizophrenia. Regarding relative abundance, little evidence of disorder specificity was found. Instead, a transdiagnostic pattern of microbiota signatures was found. Depleted levels of Faecalibacterium and Coprococcus and enriched levels of Eggerthella were consistently shared between major depressive disorder, bipolar disorder, psychosis and schizophrenia, and anxiety, suggesting these disorders are characterized by a reduction of anti-inflammatory butyrate-producing bacteria, while pro-inflammatory genera are enriched. The confounding associations of region and medication were also evaluated. CONCLUSIONS AND RELEVANCE: This systematic review and meta-analysis found that gut microbiota perturbations were associated with a transdiagnostic pattern with a depletion of certain anti-inflammatory butyrate-producing bacteria and an enrichment of pro-inflammatory bacteria in patients with depression, bipolar disorder, schizophrenia, and anxiety.
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Alcohol, microbiome, and their effect on psychiatric disorders.
There is accumulating evidence that alcohol consumption and especially alcohol withdrawal increase brain levels of known innate immune signaling molecules and cause neuroinflammation. It has been shown that microbiota play a pivotal role in this process and affect central neurochemistry and behavior. Disruption of or alterations in the intimate cross-talk between microbiome and brain may be a significant factor in many psychiatric disorders. Alterations in the composition of the microbiome, so called dysbiosis, may result in detrimental distortion of microbe-host homeostasis modulating the hypothalamic-pituitary-adrenal axis. A variety of pathologies are associated with changes in the community structure and function of the gut microbiota, suggesting a link between dysbiosis and disease etiology, including irritable bowel syndrome depression, anxiety disorders, schizophrenia, and alcoholism. Despite a paucity of clinical studies in alcohol-dependent humans, emerging data suggests that alcohol induced alterations of the microbiome may explain reward-seeking behaviors as well as anxiety, depression, and craving in withdrawal and increase the risk of developing psychiatric disorders.
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Cross-kingdom gut microbiota signatures and their associations with clinical phenotypes in adolescents with bipolar depression.
Emerging evidence highlights the pivotal role of the gut microbiota (GM) in mental health; however, investigations into its cross-kingdom composition in adolescent bipolar disorder remain critically limited. Most studies have focused solely on bacteria, overlooking the complex interactions involving archaea, viruses, and fungi. This study aimed to comprehensively characterize the taxonomic and functional alterations in the cross-kingdom gut microbiota of adolescents with bipolar depression and examine their associations with clinical parameters. We enrolled 60 adolescents aged 12-18 years, including 30 diagnosed with bipolar depression and 30 age- and sex-matched healthy controls. Fecal samples were collected alongside detailed clinical data, including psychiatric symptomatology, cognitive assessments, and dietary habits. Metagenomic sequencing was conducted to profile microbial taxa and functional gene pathways across domains. Statistical analyses assessed differences in alpha and beta diversity, differential abundance, and correlations with clinical phenotypes. Alpha diversity was significantly reduced in the viral and fungal domains among patients, while archaeal and bacterial diversity showed no significant differences. Beta diversity analysis did not reveal global community structural shifts across domains. Taxonomic profiling identified Methanohalobium evestigatum as significantly enriched in archaea, alongside increased abundance of several Firmicutes and Actinobacteria species in the bacterial domain. Viral analysis revealed elevated levels of Brussowvirus AlQ132, Orpheovirus IHUMI LCC2, Afonbuvirus coli, Carjivirus hominis, and Carjivirus communis in the patient group. LEfSe analysis uncovered 15 significantly altered metabolic pathways, including those involved in DNA repair, energy metabolism, and immune signaling. Notably, several taxa and pathways were significantly associated with clinical parameters such as symptom severity, cognitive flexibility, sleep quality, and dietary intake. Adolescents with bipolar depression exhibit distinct alterations in cross-kingdom gut microbiota composition and function, with specific microbial taxa and metabolic pathways correlating with key clinical phenotypes. These findings underscore the potential of gut microbiome signatures as biomarkers and therapeutic targets in early-onset mood disorders and highlight the importance of including archaea, fungi, and viruses in future microbiome-based mental health research.
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Effects of Vancomycin on Persistent Pain-Stimulated and Pain-Depressed Behaviors in Female Fischer Rats With or Without Voluntary Access to Running Wheels.
The present experiments determined the effects of the narrow-spectrum antibiotic vancomycin on inflammatory pain-stimulated and pain-depressed behaviors in rats. Persistent inflammatory pain was modeled using dilute formalin (0.5%). Two weeks of oral vancomycin administered in drinking water attenuated Phase II formalin pain-stimulated behavior, and prevented formalin pain-depressed wheel running. Fecal microbiota transplantation produced a non-significant trend toward reversal of the vancomycin effect on pain-stimulated behavior. Vancomycin depleted Firmicutes and Bacteroidetes populations in the gut while having a partial sparing effect on Lactobacillus species and Clostridiales. The vancomycin treatment effect was associated with an altered profile in amino acid concentrations in the gut with increases in arginine, glycine, alanine, proline, valine, leucine, and decreases in tyrosine and methionine. These results indicate that vancomycin may have therapeutic effects against persistent inflammatory pain conditions that are distal to the gut. PERSPECTIVE: The narrow-spectrum antibiotic vancomycin reduces pain-related behaviors in the formalin model of inflammatory pain. These data suggest that manipulation of the gut microbiome may be one method to attenuate inflammatory pain amplitude.
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Affective disorders impact prevalence of Flavonifractor and abundance of Christensenellaceae in gut microbiota.
Background Affective disorders (AD) have been associated with a higher prevalence of the gut Flavonifractor genus and a lower abundance of the gut Christensenellaceae family. Objective and methods By pooling two independent study samples of patients with AD (n = 176), their unaffected first-degree relatives (n = 70) and healthy controls (n = 101) we aimed to replicate and extend our prior findings of differential Flavonifractor prevalence and Christensenellaceae abundance when comparing patients with AD and healthy controls. The gut microbiota was profiled using 16S rRNA gene amplicon sequencing. Results The pattern of higher prevalence of Flavonifractor and lower Centered Log-Ratio (CLR) abundance of Christensenellaceae was associated with AD. In generalized linear models the CLR abundance of Christensenellaceae was lower in patients with AD (p = 0.024), and in smokers (p = 1.9*10-4), and inversely associated with increasing waist circumference (p = 0.031). The prevalence of Flavonifractor was higher in patients with AD (p = 0.033) and in smokers (p = 0.036). No impact of psychotropic medication was found. The CLR abundance of Christensenellaceae (p = 0.041), but not the prevalence of Flavonifractor (p = 0.20) could distinguish non-smoking patients with AD from non-smoking healthy controls, whereas no such associations were found in smokers. Unaffected relatives neither differed from patients with AD nor from healthy controls. Conclusion Compared with findings in healthy controls, AD was associated with a significantly lower CLR abundance of the health-linked Christensenellaceae and a significantly higher prevalence of Flavonifractor; findings that are associated with enhanced oxidative stress and systemic low-grade inflammation. If our observations are validated in future independent studies, they support the notion that parts of aberrant gut microbiota are shared by AD and states of dysmetabolism.