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Exploring the Link Between the Gut Microbiota and Epigenetic Factors in Anorexia Nervosa.
OBJECTIVE: Anorexia nervosa (AN) is an often chronic eating disorder that involves genetic, neurohormonal, and epigenetic factors along with key contributions from the microbiota-gut-brain axis. However, interactions between these factors are poorly understood. Recent studies have emphasized the microbiota-gut-brain axis and epigenetic changes as potentially important contributors to AN. Exploring these interactions may improve understanding of the etiology and persistence of AN. METHODS: Studies specifically addressing microbial-epigenetic interactions in AN remain limited. However, similar associations have been documented in related disorders such as obesity and depression, providing potential models for AN research. RESULTS: Research in obesity has shown that dietary factors influence the composition of the gut microbiota and subsequent epigenetic modifications, affecting metabolic parameters and disease progression. Similarly, in depression, microbially produced metabolites influence brain function and epigenetic processes, contributing to neuropsychiatric symptoms. In AN, altered microbial composition may affect weight regulation and epigenetic patterns. Therapies targeting the microbiome, such as fecal microbiota transplantation, are under investigation for AN, highlighting the potential therapeutic utility of ameliorating microbial dysbiosis. DISCUSSION: This article highlights the importance of investigating microbial-epigenetic interactions in AN. By drawing parallels with obesity and depression, we aim to deepen our understanding of AN mechanisms and ultimately improve patient outcomes.
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Oral treatment with Lactobacillus reuteri attenuates depressive-like behaviors and serotonin metabolism alterations induced by chronic social defeat stress.
BACKGROUND: Alterations in bidirectional gut-brain interactions are believed to be involved in the pathogenesis of neuropsychiatric diseases. Considering the putative connections among gut microbiota, neural function, and behavior, this study investigated the potential of microbe-induced gut-to-brain signaling to modulate the impact of stress on depressive-like behaviors and serotonin metabolism. METHODS: Depression-susceptible mice induced by chronic social defeat stress received oral treatment of either Lactobacillus reuteri 3 (L. reuteri 3) or vehicle for 28 days, and alterations in behavior and serotonin metabolism were assessed. 16S rRNA sequencing and gas chromatograph were employed to analyze the gut microbiota community and short-chain fatty acids (SCFAs). RESULTS: Treatment with L. reuteri 3 ameliorated depressive-like behaviors, suppressed the increase in the relative abundances of Clostridiales and Adlercreutzia, improved the decrease in abundances of Lactobacillus, Allobaculum, and Sutterella induced by stress, and significantly increased the proportion of Bifidobacterium. L. reuteri 3 reduced the acetate and total SCFAs levels in the depression group. Blood and colon 5-HT were decreased in depressive-like mice but were significantly ameliorated after L. reuteri 3 treatment. Moreover, L. reuteri 3 administration increased the expression of enzymes involved in serotonin biosynthesis but suppressed that of the enzymes involved in tryptophan metabolism along the kynurenine pathway in colon and prefrontal cortex. CONCLUSIONS: Despite the complexity of the gut microbiota, exposure to a single microbial strain L. reuteri 3 can protect against depressive-like behaviors induced by chronic social defeat stress. The anti-depressive effects of L. reuteri 3 were associated with improved gut microbiota and serotonin metabolism.
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Antibiotic-induced microbiome depletion is associated with resilience in mice after chronic social defeat stress.
BACKGROUND: The brain-gut axis plays a role in the pathogenesis of stress-related disorders such as depression. However, the role of brain-gut axis in the resilience versus susceptibility after stress remains unclear. Here, we examined the effects of antibiotic-induced microbiome depletion on an anhedonia-like phenotype in adult mice subjected to chronic social defeat stress (CSDS). METHODS: Using CSDS paradigm, we investigated the effects of antibiotic-induced microbiome depletion on the resilience versus susceptibility in mice. RESULTS: Treatment with an antibiotic cocktail for 14 days significantly decreased the diversity and composition of the microbiota in the host gut. Proteobacteria were markedly increased after treatment with the antibiotic cocktail. At the genus and species levels, the antibiotic-treated group exhibited marked alterations in the microbiota compared with a control group. CSDS was shown to significantly improve the abnormal composition of gut microbiota in the antibiotic-treated group. CSDS did not produce an anhedonia-like phenotype in the antibiotic-treated mice, but did induce an anhedonia-like phenotype in control mice, suggesting that gut bacteria are essential for the development of CSDS-induced anhedonia. CSDS treatment did not alter the plasma levels of interleukin-6 or the expression of synaptic proteins, such as PSD-95 and GluA1, in the prefrontal cortex of antibiotic-treated mice. LIMITATIONS: Specific microbiome were not determined. CONCLUSIONS: These findings suggest that antibiotic-induced microbiome depletion contributed to resilience to anhedonia in mice subjected to CSDS. Therefore, it is likely that the brain-gut axis plays a role in resilience versus susceptibility to stress.
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Stressful events induce long-term gut microbiota dysbiosis and associated post-traumatic stress symptoms in healthcare workers fighting against COVID-19.
OBJECTIVE: The microbiota-gut-brain axis is a key pathway perturbed by prolonged stressors to produce brain and behavioral disorders. Frontline healthcare workers (FHWs) fighting against COVID-19 typically experience stressful event sequences and manifest some mental symptoms; however, the role of gut microbiota in such stress-induced mental problems remains unclear. We investigated the association between the psychological stress of FHW and gut microbiota. METHODS: We used full-length 16S rRNA gene sequencing to characterize the longitudinal changes in gut microbiota and investigated the impact of microbial changes on FHWs' mental status. RESULTS: Stressful events induced significant depression, anxiety, and stress in FHWs and disrupted the gut microbiome; gut dysbiosis persisted for at least half a year. Different microbes followed discrete trajectories during the half-year of follow-up. Microbes associated with mental health were mainly Faecalibacterium spp. and [Eubacterium] eligens group spp. with anti-inflammatory effects. Of note, the prediction model indicated that low abundance of [Eubacterium] hallii group uncultured bacterium and high abundance of Bacteroides eggerthii at Day 0 (immediately after the two-month frontline work) were significant determinants of the reappearance of post-traumatic stress symptoms in FHWs. LIMITATIONS: The lack of metabolomic evidence and animal experiments result in the unclear mechanism of gut dysbiosis-related stress symptoms. CONCLUSION: The stressful event sequences of fighting against COVID-19 induce characteristic longitudinal changes in gut microbiota, which underlies dynamic mental state changes.
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Relationship between human oral microbiome dysbiosis and neuropsychiatric diseases: An updated overview.
The role of the gut-brain axis in mental health disorders has been extensively studied. As the oral cavity is the starting point of the digestive tract, the role that the oral microbiota plays in mental health disorders has gained recent attention. Oral microbiota can enter the bloodstream and trigger inflammatory responses or translocate to the brain through the trigeminal nerve or olfactory system. Hence, the concept of the oral microbiota-brain axis has emerged. Several hypotheses have been suggested that the oral microbiota can enter the gastrointestinal tract and affect the gut-brain axis; however, literature describing oral-brain communication remains limited. This review summarizes the characteristics of oral microbiota and its mechanisms associated with mental health disorders. Through a comprehensive examination of the relationship between oral microbiota and various neuropsychiatric diseases, such as anxiety, depression, schizophrenia, autism spectrum disorder, epilepsy, Parkinson's disease, and dementia, this review seeks to identify promising avenues of future research.
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Association of Alterations in Intestinal Microbiota With Impaired Psychological Function in Patients With Inflammatory Bowel Diseases in Remission.
BACKGROUND & AIMS: Depression and anxiety are frequent comorbidities with inflammatory bowel diseases (IBD). Alterations to the intestinal microbiome promote not only intestinal inflammation but also psychologic function. We studied the interactions between the composition of the intestinal microbiota and psychological outcomes in patients with IBD in Switzerland. METHODS: We performed a prospective study of psychological comorbidities and quality of life (QoL) in 171 participants in the Swiss IBD Cohort Study with IBD in remission. Participants complete the Hospital Anxiety and Depression Scale, Perceived Stress Questionnaire, the 36-Item Short Form Survey, and the IBD QoL Questionnaire. Microbes were collected from intestinal biopsies and analyzed by 16S rRNA high-throughput sequencing. RESULTS: Microbiomes of patients with higher perceived stress had significantly lower alpha diversity. Anxiety and depressive symptoms were significantly associated with beta diversity. We found a negative correlation between psychological distress and abundance of Clostridia, Bacilli, Bacteroidia, and Beta- and Gamma-proteobacteria. Psychological distress was also associated with decreases in operational taxonomic units from the lineages of Lachnospiraceae, Fusobacteriaceae, Ruminococcaceae, Veillonellaceae, Alcaligenaceae, Desulfovibrionaceae, and Bacteroidaceae families. The relative abundance of Bifidobacterium in patients with Crohn's disease and Desulfovibrio in patients with ulcerative colitis correlated with depression, whereas abundance of Sutterella, RF 32, and Lactococcus correlated with quality of life in patients with Crohn's disease. CONCLUSIONS: We identified correlations between the composition of the intestinal microbiota in patients with IBD and remission, psychological well-being, and QoL. Further studies should investigate how intestinal inflammation, the microbiome, and microbial metabolites affect psychological well-being and whether these components are mono- or bi-directionally linked.
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Metabolomics analysis of microbiota-gut-brain axis in neurodegenerative and psychiatric diseases.
Gut microbiota represents a complex physiological ecosystem that influences the host health. Alterations in the microbiome metabolism affect the body homeostasis and they have been associated with the development of different human neurodegenerative and neuropsychiatric disorders, such as Alzheimer's disease, autism spectrum disorder, bipolar disorder, depression, Huntington's disease, Parkinson's disease, posttraumatic stress disorder and schizophrenia. The development of these complex diseases is influenced by various factors, including genetic predisposition and environmental triggers. Gut microbiota has recently emerged as an important actor in their physiopathology that has been shown to play a role in inflammation, oxidative stress, and gut permeability. Therefore, targeting the metabolites that are produced by or associated with the gut microbiota may help us understand how imbalance in the gut-brain axis affects human health. This review offers a comprehensive overview of the literature on this matter, offering the readers an insight in the state-of-art metabolic measurements of the gut-brain axis in various brain-related diseases.
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Fibromyalgia pain may have a gut solution.
In this issue of Neuron, Cai et al.1 demonstrated that transferring fecal microbiota from fibromyalgia patients to mice confers pain hypersensitivity and depression-like behavior, which is reversed by fecal microbiota transplant from healthy donors. Fibromyalgia patients experience significant symptom relief after fecal microbiota transplantation.
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Ingestion of probiotic (Lactobacillus helveticus and Bifidobacterium longum) alters intestinal microbial structure and behavioral expression following social defeat stress.
Social stress exacerbates anxious and depressive behaviors in humans. Similarly, anxiety- and depressive-like behaviors are triggered by social stress in a variety of non-human animals. Here, we tested whether oral administration of the putative anxiolytic probiotic strains Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 reduces the striking increase in anxiety-like behavior and changes in gut microbiota observed following social defeat stress in Syrian hamsters. We administered the probiotic at two different doses for 21 days, and 16S rRNA gene amplicon sequencing revealed a shift in microbial structure following probiotic administration at both doses, independently of stress. Probiotic administration at either dose increased anti-inflammatory cytokines IL-4, IL-5, and IL-10 compared to placebo. Surprisingly, probiotic administration at the low dose, equivalent to the one used in humans, significantly increased social avoidance and decreased social interaction. This behavioral change was associated with a reduction in microbial richness in this group. Together, these results demonstrate that probiotic administration alters gut microbial composition and may promote an anti-inflammatory profile but that these changes may not promote reductions in behavioral responses to social stress.
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Endocannabinoid system mediates the association between gut-microbial diversity and anhedonia/amotivation in a general population cohort.
Anhedonia and amotivation are debilitating symptoms and represent unmet therapeutic needs in a range of clinical conditions. The gut-microbiome-endocannabinoid axis might represent a potential modifiable target for interventions. Based on results obtained from animal models, we tested the hypothesis that the endocannabinoid system mediates the association between gut-microbiome diversity and anhedonia/amotivation in a general population cohort. We used longitudinal data collected from 786 volunteer twins recruited as part the TwinsUK register. Our hypothesis was tested with a multilevel mediation model using family structure as random intercept. The model was set using alpha diversity (within-individual gut-microbial diversity) as predictor, serum and faecal levels of the endocannabinoid palmitoylethanolamide (PEA) as mediator, and anhedonia/amotivation as outcome. PEA is considered the endogenous equivalent of cannabidiol, with increased serum levels believed to have anti-depressive effects, while increased stool PEA levels, reflecting increased excretion, are believed to have opposite, detrimental, effects on mental health. We therefore expected that either reduced serum PEA or increased stool PEA would mediate the association between microbial diversity and anhedonia amotivation. Analyses were adjusted for obesity, diet, antidepressant use, sociodemographic and technical covariates. Data were imputed using multiple imputation by chained equations. Mean age was 65.2 ± 7.6; 93% of the sample were females. We found a direct, significant, association between alpha diversity and anhedonia/amotivation (β = -0.37; 95%CI: -0.71 to -0.03; P = 0.03). Faecal, but not serum, levels of the endocannabinoid palmitoylethanolamide (PEA) mediated this association: the indirect effect was significant (β = -0.13; 95%CI: -0.24 to -0.01; P = 0.03), as was the total effect (β = -0.38; 95%CI: -0.72 to -0.04; P = 0.03), whereas the direct effect of alpha diversity on anhedonia/amotivation was attenuated fully (β = -0.25; 95%CI: -0.60 to 0.09; P = 0.16). Our results suggest that gut-microbial diversity might contribute to anhedonia/amotivation via the endocannabinoid system. These findings shed light on the biological underpinnings of anhedonia/amotivation and suggest the gut microbiota-endocannabinoid axis as a promising therapeutic target in an area of unmet clinical need.