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Prophylactic Effects of Bifidobacterium adolescentis on Anxiety and Depression-Like Phenotypes After Chronic Stress: A Role of the Gut Microbiota-Inflammation Axis.
Stress disturbs the balance of the gut microbiota and stimulates inflammation-to-brain mechanisms. Moreover, stress leads to anxiety and depressive disorders. Bifidobacterium adolescentis displays distinct anti-inflammatory effects. However, no report has focused on the anxiolytic and antidepressant effects of B. adolescentis related to the gut microbiome and the inflammation on chronic restraint stress (CRS) in mice. We found that pretreatment with B. adolescentis increased the time spent in the center of the open field apparatus, increased the percentage of entries into the open arms of the elevated plus-maze (EPM) and the percentage of time spent in the open arms of the EPM, and decreased the immobility duration in the tail suspension test as well as the forced swimming test (FST). Moreover, B. adolescentis increased the sequence proportion of Lactobacillus and reduced the sequence proportion of Bacteroides in feces. Furthermore, B. adolescentis markedly reduced the protein expression of interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α), p-nuclear factor-kappa B (NF-κB) p65 and Iba1 and elevated brain derived neurotrophic factor (BDNF) expression in the hippocampus. We conclude that the anxiolytic and antidepressant effects of B. adolescentis are related to reducing inflammatory cytokines and rebalancing the gut microbiota.
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Gut bacterial taxonomic abundances vary with cognition, personality, and mood in the Wisconsin Longitudinal Study.
Animal studies have shown that the gut microbiome can influence memory, social behavior, and anxiety-like behavior. Several human studies show similar results where variation in the gut microbiome is associated with dementia, depression, and personality traits, though most of these studies are limited by small sample size and other biases. Here, we analyzed fecal samples from 313 participants in the Wisconsin Longitudinal Study, a randomly selected population-based cohort of older adults, with measured psycho-cognitive dimensions (cognition, mood, and personality) and key confounders. 16s V4 sequencing showed that Megamonas is associated with all measured psycho-cognitive traits, Fusobacterium is associated with cognitive and personality traits, Pseudoramibacter_Eubacterium is associated with mood and personality traits, Butyvibrio is associated with cognitive traits, and Cloacibacillus is associated with mood traits. These findings are robust to sensitivity analyses and provide novel evidence of shared relationships between the gut microbiome and multiple psycho-cognitive traits in older adults, confirming some of the animal literature, while also providing new insights. While we addressed some of the weaknesses in prior studies, further studies are necessary to elucidate temporal and causal relationships between the gut microbiome and multiple psycho-cognitive traits in well-phenotyped, randomly-selected population-based samples.
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Examining the immunoepigenetic-gut microbiome axis in the context of self-esteem among Native Hawaiians and other Pacific Islanders.
Introduction: Native Hawaiian and other Pacific Islander (NHPI) populations experience higher rates of immunometabolic diseases compared to other racial-ethnic groups in Hawaii. As annual NHPI mortality rates for suicide and type 2 diabetes mellitus (T2DM) exceed those of the state as a whole, understanding the social and biological mechanisms underlying these disparities are urgently needed to enable preventive strategies. Methods: A community-based approach was used to investigate the immunoepigenetic-gut microbiome axis in an NHPI-enriched cohort of Oahu residents (N = 68). Self-esteem (SE) data was collected using a modified Rosenberg self-esteem (SE) assessment as a proxy measure for mental wellbeing in consideration for cultural competency. T2DM status was evaluated using point-of-care A1c (%) tests. Stool samples were collected for 16s-based metagenomic sequencing analyses. Plasma from blood samples were isolated by density-gradient centrifugation. Peripheral blood mononuclear cells (PBMCs) were collected from the same samples and enriched for monocytes using negative selection techniques. Flow-cytometry was used for immunoprofiling assays. Monocyte DNA was extracted for Illumina EPIC array-based methylation analysis. Results: Compared to individuals with normal SE (NSE), those with low SE (LSE) exhibited significantly higher plasma concentrations (pg/ml) of proinflammatory cytokines IL-8 (p = 0.051) and TNF-α (p = 0.011). Metagenomic analysis revealed that the relative abundance (%) of specific gut bacteria significantly differed between SE groups - some of which directly correlated with SE scores. Gene ontology analysis revealed that 104 significantly differentially methylated loci (DML) between SE groups were preferentially located at genes involved in immunometabolic processes. Horvath clock analyses indicated epigenetic age (Epi-Age) deceleration in individuals with LSE and acceleration in individuals with NSE (p = 0.042), yet was not reproduced by other clocks. Discussion: These data reveal novel differences in the immunoepigenetic-gut microbiome axis with respect to SE, warranting further investigation into its relationship to brain activity and mental health in NHPI. Unexpected results from Epi-Age analyses warrant further investigation into the relationship between biological age and disparate health outcomes among the NHPI population. The modifiable component of epigenetic processes and the gut microbiome makes this axis an attractive target for potential therapeutics, biomarker discovery, and novel prevention strategies.
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Gut-Mind Interactions in Psychedelic Healing: A Case Study Assessing the Effects of Huachuma and Ayahuasca on the Mind and Microbiome.
BACKGROUND: Psychedelic plant medicines such as Ayahuasca and Huachuma (San Pedro cactus) are gaining scientific attention for their potential to improve mental health. However, the interplay between these traditional medicines, the gut microbiome, and mental health outcomes remains underexplored. OBJECTIVE: The main objectives of this study are to investigate the effects of Ayahuasca and Huachuma ceremonies on the gut microbiome, depression, and subjective connectedness in a single patient and to generate hypotheses for future studies. CASE: A 35-year-old female with prior psychedelic experience participated in separate Ayahuasca and Huachuma ceremonies. Qualitative data were collected through patient interviews. Quantitative data included stool samples collected before and after each ceremony for microbiome analysis, as well as survey data using the Hamilton Depression Rating Scale (HAM-D) and Watts Connectedness Scale (WCS) administered pre- and post-ceremony. RESULTS: Both ceremonies resulted in substantial reductions in depression scores (HAM-D decreased: Ayahuasca from 18 to 6; Huachuma from 12 to 2) and connectedness scores (WCS increased: Ayahuasca from 62.3% to 95.37%; Huachuma from 58.32% to 84.65%). Although Ayahuasca and Huachuma induced different gut microbial composition shifts, reductions in pro-inflammatory taxa, normalization of inflammation-linked bacterial species, and increases in beneficial butyrate-producing bacterial species were observed for both. These microbial shifts aligned with improved subjective mental health and reduced inflammation. Qualitative interviews revealed distinct archetypal experiences with each medicine, informing personalized therapeutic approaches. CONCLUSION: This hypothesis-generating case study illustrates a potential link between psychedelic-induced microbiome changes and improvements in mental health which may contribute to reduced inflammation and sustained antidepressant effects via the microbiota-gut-brain axis.
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Mechanisms of Maternal Diet-Induced Obesity Affecting the Offspring Brain and Development of Affective Disorders.
Depression and metabolic disease are common disorders that share a bidirectional relationship and continue to increase in prevalence. Maternal diet and maternal behaviour both profoundly influence the developmental trajectory of offspring during the perinatal period. At an epidemiological level, both maternal depression and obesity during pregnancy have been shown to increase the risk of neuropsychiatric disease in the subsequent generation. Considerable progress has been made to understand the mechanisms by which maternal obesity disrupts the developing offspring gut-brain axis, priming offspring for the development of affective disorders. This review outlines such mechanisms in detail, including altered maternal care, the maternal microbiome, inflammation, breast milk composition, and maternal and placental metabolites. Subsequently, offspring may be prone to developing gut-brain interaction disorders with concomitant changes to brain energy metabolism, neurotransmission, and behaviour, alongside gut dysbiosis. The gut microbiome may act as a key modifiable, and therefore treatable, feature of the relationship between maternal obesity and the offspring brain function. Further studies examining the relationship between maternal nutrition, the maternal microbiome and metabolites, and offspring neurodevelopment are warranted to identify novel therapeutic targets.
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Stress-induced obesity in mice causes cognitive decline associated with inhibition of hippocampal neurogenesis and dysfunctional gut microbiota.
Effects of stress on obesity have been thoroughly studied in high-fat diet fed mice, but not in normal diet fed mice, which is important to clarify because even on a normal diet, some individuals will become obese under stress conditions. Here we compared mice that showed substantial weight gain or loss under chronic mild stress while on a normal diet; we compared the two groups in terms of cognitive function, hypothalamic-pituitary-adrenal signaling, neurogenesis and activation of microglia in hippocampus, gene expression and composition of the gut microbiome. Chronic mild stress induced diet-independent obesity in approximately 20% of animals, and it involved inflammatory responses in peripheral and central nervous system as well as hyperactivation of the hypothalamic-pituitary-adrenal signaling and of microglia in the hippocampus, which were associated with cognitive deficits and impaired hippocampal neurogenesis. It significantly increased in relative abundance at the phylum level (Firmicutes), at the family level (Prevotellaceae ucg - 001 and Lachnospiraceae NK4a136), at the genus level (Dubosiella and Turicibacter) for some enteric flora, while reducing the relative abundance at the family level (Lactobacillaceae and Erysipelotrichaceae), at the genus level (Bacteroidota, Alistipes, Alloprevotella, Bifidobacterium and Desulfovibrio) for some enteric flora. These results suggest that stress, independently of diet, can induce obesity and cognitive decline that involve dysfunctional gut microbiota. These insights imply that mitigation of hypothalamic-pituitary-adrenal signaling and microglial activation as well as remodeling of gut microbiota may reverse stress-induced obesity and associated cognitive decline.
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Leaky Gut, Leaky Brain?
'Leaky gut' syndrome, long-associated with celiac disease, has attracted much attention in recent years and for decades, was widely known in complementary/alternative medicine circles. It is often described as an increase in the permeability of the intestinal mucosa, which could allow bacteria, toxic digestive metabolites, bacterial toxins, and small molecules to 'leak' into the bloodstream. Nervous system involvement with celiac disease is know to occur even at subclinical levels. Gluten and gluten sensitivity are considered to trigger this syndrome in individuals genetically predisposed to celiac disease. However, the incidence of celiac disease in the general population is quite low. Nevertheless, increased public interest in gluten sensitivity has contributed to expanded food labels stating 'gluten-free' and the proliferation of gluten-free products, which further drives gluten-free lifestyle changes by individuals without frank celiac disease. Moreover, systemic inflammation is associated with celiac disease, depression, and psychiatric comorbidities. This mini-review focuses on the possible neurophysiological basis of leaky gut; leaky brain disease; and the microbiota's contribution to inflammation, gastrointestinal, and blood-brain barrier integrity, in order to build a case for possible mechanisms that could foster further 'leaky' syndromes. We ask whether a gluten-free diet is important for anyone or only those with celiac disease.
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Methamphetamine Disturbs Gut Homeostasis and Reshapes Serum Metabolome, Inducing Neurotoxicity and Abnormal Behaviors in Mice.
As an illicit psychostimulant, repeated methamphetamine (MA) exposure results in addiction and causes severe neurotoxicity. Studies have revealed complex interactions among gut homeostasis, metabolism, and the central nervous system (CNS). To investigate the disturbance of gut homeostasis and metabolism in MA-induced neurotoxicity, 2 mg/kg MA or equal volume saline was intraperitoneally (i.p.) injected into C57BL/6 mice. Behavioral tests and western blotting were used to evaluate neurotoxicity. To determine alterations of colonic dysbiosis, 16s rRNA gene sequencing was performed to analyze the status of gut microbiota, while RNA-sequencing (RNA-seq) and Western Blot analysis were performed to detect colonic damage. Serum metabolome was profiled by LC-MS analysis. We found that MA induced locomotor sensitization, depression-, and anxiety-like behaviors in mice, along with dysfunction of the dopaminergic system and stimulation of autophagy as well as apoptosis in the striatum. Notably, MA significantly decreased microbial diversity and altered the component of microbiota. Moreover, findings from RNA-seq implied stimulation of the inflammation-related pathway after MA treatment. Western blotting confirmed that MA mediated colonic inflammation by activating the TLR4-MyD88-NF-κB pathway and impaired colonic barrier. In addition, serum metabolome was reshaped after MA treatment. Specifically, bacteroides-derived sphingolipids and serotonin were obviously altered, which were closely correlated with locomotor sensitization, depression-, and anxiety-like behaviors. These findings suggest that MA disrupts gut homeostasis by altering its microbiome and arousing inflammation, and reshapes serum metabolome, which provide new insights into understanding the interactions between gut homeostasis and MA-induced neurotoxicity.
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The effect of pectin supplementation on geriatric individuals with frailty: a randomised placebo-controlled dietary intervention study.
Frailty is associated with impaired physical function, psychological decline, and alterations in the gut microbiome, yet nutritional strategies targeting these interconnected pathways remain limited. Low-methoxy (LM) pectin, a fermentable dietary fibre derived from plant cell walls, has demonstrated immunomodulatory and microbiome-modifying effects in preclinical studies, but evidence in older adults with frailty is scarce. We conducted a 4-week double-blind, randomised, placebo-controlled trial evaluating LM pectin supplementation in older adults with frailty. Thirty-one participants were enrolled, and 29 completed the intervention. Physical performance, psychological well-being, quality of life, inflammatory biomarkers, and gut microbiome composition were assessed at baseline and follow-up. Compared with placebo, low-methoxy pectin supplementation significantly improved lower limb function measured by the 30-second sit-to-stand test (2.07 ± 1.94 vs 0.71 ± 2.27 repetitions; p = 0.038), while no significant changes were observed in Timed Up and Go performance. Supplementation also reduced anxiety and depression scores and improved several Short Form-36 domains, including physical functioning, vitality, mental health, and social functioning. No significant differences were detected in circulating inflammatory biomarkers. Gut microbiome analysis demonstrated increased relative abundance of Coprococcus comes, an acetate-producing species linked to gut-brain signalling and psychological health. These findings provide preliminary evidence that LM pectin supplementation may improve physical and psychological outcomes and alter gut microbial composition in older adults with frailty. Larger, adequately powered trials are needed to determine whether these changes are reproducible and to investigate potential microbiome-related mechanisms. Trial registration number: NCT06955975 ( https://clinicaltrials.gov/study/NCT06955975 ; Clinical Trials.gov; 2025-06-22).
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A protocol for the Teen Bugs study: An integrative, multi-omics approach to understanding the role of the gut microbiome and mesocorticolimbic system in adolescent mental health following early adverse caregiving.
Caregiving-related early adversities (crEAs) are potent risk factors for the development of internalizing psychopathology (e.g., depression, anxiety). Alterations to the dopaminergic mesocorticolimbic system, which supports the construction of reward-related experiences, are commonly observed following crEA exposure and are thought to mediate this risk. Indeed, many internalizing disorders are characterized by disruptions in how reward-related information is represented and used to guide affective and motivational states. Critically, the effects of crEA on mesocorticolimbic functioning may be shaped by input from peripheral systems, such as the gut microbiome, though such bottom-up signaling has been markedly understudied in humans. The Teen Bugs study was thus developed to identify gut microbiome-dependent metabolic pathways linking crEA exposure to mesocorticolimbic functioning and internalizing symptoms in adolescents, a group that experiences a disproportionate incidence of psychopathology relative to other age groups and is underrepresented in the gut microbiome literature. Adolescents aged 12-15 years, with and without histories of crEA exposure, will be followed across three timepoints over five years. At each timepoint, participants will complete a semi-structured clinical interview, a reward-guided decision-making task, and self-report questionnaires assessing mental health, previous caregiving experiences, reward-related behaviors, as well as developmental and lifestyle factors. Participants will also undergo multimodal neuroimaging that leverages MRI-based proxy markers of dopaminergic neurobiology and provide stool and blood samples for metagenomic and metabolomic profiling, respectively. This integrative design has the potential to clarify developmentally salient mechanisms that may serve as novel therapeutic targets for youth most at risk of, or already experiencing, internalizing psychopathology.