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Bridging the gut and mind: a narrative review of depression in Crohn's disease and emerging gut-brain axis therapies.
Depression is a highly prevalent and clinically significant comorbidity in Crohn's disease (CD), a form of inflammatory bowel disease (IBD), and is associated with increased disease activity, hospitalization, and a reduced quality of life (QoL). While traditionally attributed to the psychosocial burden of chronic illness, emerging evidence indicates that depressive symptoms in CD arise from dysregulation of the gut-brain axis (GBA), a bidirectional network linking immune, microbial, and central nervous system (CNS) processes. Chronic intestinal inflammation, characterized by elevated cytokines such as tumor necrosis factor (TNF-α) and interleukin-6 (IL-6), may influence brain function through vagal signaling, hypothalamic-pituitary-adrenal (HPA) axis activation, and neuroimmune pathways. Concurrently, epithelial barrier dysfunction and microbial dysbiosis promote translocation of bacterial products, further amplifying systemic inflammation and neuroimmune signaling. This review consolidates preclinical and clinical evidence linking immune activation, microbial alterations, and neuroimmune signaling to depression in CD. The review compares emerging therapeutic strategies, such as ketamine enantiomers, vagus nerve stimulation, and microbiota-targeting natural compounds, with established therapies like serotonergic antidepressants, cognitive behavioral therapy, and biologic immunotherapies. Across these modalities, therapeutic effects on mood are heterogeneous and often dissociated from improvements in intestinal inflammation, highlighting the multifunctional nature of GBA dysfunction. Overall, these findings suggest that therapeutic responses in CD-associated depression may depend on the extent to which interventions modulate distinct components of the GBA, including immune, neural, and microbial pathways. These observations emphasize the need for integrative treatment strategies that address the multiple contributors of GBA dysbiosis. Future studies incorporating standardized and emerging psychiatric, immunological, and microbiome outcomes will be critical to identifying mechanisms for specific treatment responses in this population.
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Polyphenol intake and depressive symptoms in young adults: evidence from a population-based longitudinal study.
Due to the high prevalence of depression among young adults, identifying prevention strategies during young adulthood is crucial. Dietary polyphenols have been associated with depression in older cohorts; however, the association remains unclear, particularly in young adults. This study aimed to assess the prospective association between the intake of total polyphenols, polyphenol classes and polyphenol subclasses with depressive symptoms in young adults. Data from 1484 Raine Study Generation 2 participants (52·7 % female; baseline mean age (sd): 20 (0·5)) at the -20, -22, and -27 year follow-ups (n 964, 979 and 1094, respectively), with overlap across follow-ups, were used. Energy-adjusted polyphenol intake was estimated from FFQ data using our expansion of the AUSNUT 2011-13 and Phenol-Explorer to include polyphenol content data and categorised into quartiles. The primary outcome was self-reported depressive symptoms assessed via the twenty-one-item Depression, Anxiety and Stress Scale averaged across the three time points. Linear mixed-effects models were used to assess the association between the polyphenol intake exposures and depressive symptoms. Sociodemographic characteristics and lifestyle- and health-related behaviours were adjusted for. Participants in the highest quartiles for flavonol and hydroxybenzoic acid intake had lower depressive symptoms across time than participants in the lowest quartiles (flavonols (Q4 v. Q1 mean difference: -1.38; 95% CI -2.48, -0.28); hydroxybenzoic acids (Q4 v. Q1: -1.40; 95% CI -2.53, -0.27). We found no evidence of a highest v. lowest association for all other polyphenol categories. Future studies are required to investigate whether increasing polyphenol intake could protect against depression in young adults.
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Chronic Sleep Deprivation Causes Anxiety, Depression and Impaired Gut Barrier in Female Mice-Correlation Analysis from Fecal Microbiome and Metabolome.
BACKGROUND: Chronic sleep deprivation (CSD) plays an important role in mood disorders. However, the changes in the gut microbiota and metabolites associated with CSD-induced anxiety/depression-like behavior in female mice have not been determined. Due to the influence of endogenous hormone levels, females are more susceptible than males to negative emotions caused by sleep deprivation. Here, we aim to investigate how CSD changes the gut microbiota and behavior and uncover the relationship between CSD and gut microbiota and its metabolites in female mice. METHODS: We used a 48-day sleep deprivation (SD) model using the modified multiple platform method (MMPM) to induce anxiety/depression-like behavior in female C57BL/6J mice and verified our results using the open field test, elevated plus maze, novel object recognition test, forced swim test, and tail suspension test. We collected fecal samples of mice for 16S rDNA sequencing and untargeted metabolomic analysis and colons for histopathological observation. We used Spearmen analysis to find the correlations between differential bacterial taxa, fecal metabolites, and behaviors. RESULTS: Our study demonstrates that CSD induced anxiety/depressive-like behaviors in female mice. The results of 16S rDNA sequencing suggested that the relative abundance of the harmful bacteria g_ Rothia, g_ Streptococcus, g_ Pantoea, and g_ Klebsiella were significantly increased, while the beneficial bacteria g_ Rikenella, g_ Eubacterium]-xylanophilum-group, and g_ Eisenbergiella were significantly decreased after SD. Glycerophospholipid metabolism and glutathione metabolism were identified as key pathways in the fecal metabolism related to oxidative stress and inflammatory states of the intestine. Histological observation showed hyperplasia of epithelial cells, a decrease in goblet cells, and glandular atrophy of the colon in SD mice. There were correlations between some of the differential bacterial taxa, fecal metabolites, and behaviors. CONCLUSION: In summary, we found that CSD induced anxiety/depression-like behavior, caused gut microbiota dysbiosis, altered fecal metabolism, and damaged the colon barrier in female mice.
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Dietary resistant starch alleviates Escherichia coli-induced bone loss in meat ducks by promoting short-chain fatty acid production and inhibiting Malt1/NF-κB inflammasome activation.
BACKGROUND: Escherichia coli (E. coli) infection in humans and animals usually comes with gut dysbiosis, which is potential culprit to skeletal health, it is still unclear to whether diet interfered gut microbiome changes can be a protective strategy to bone loss development. Here, the effects of resistant starch from raw potato starch (RPS), a type of prebiotic, on E. coli-induced bone loss and gut microbial composition in meat ducks were evaluated. RESULTS: The results showed that dietary 12% RPS treatment improved bone quality, depressed bone resorption, and attenuated the pro-inflammatory reaction in both ileum and bone marrow. Meanwhile, the 12% RPS diet also increased the abundance of Firmicutes in E. coli-treated birds, along with higher production of short-chain fatty acids (SCFAs) especially propionate and butyrate. Whereas addition of β-acid, an inhibitor of bacterial SCFAs production, to the drinking water of ducks fed 12% RPS diet significantly decreased SCFAs level in cecum content and eliminated RPS-induced tibial mass improvement. Further, treatment with MI-2 to abrogate mucosa-associated lymphoid tissue lymphoma translocation protein 1 (Malt1) activity replicated the protective role of dietary 12% RPS in E. coli-induced bone loss including reduced the inhibition on nuclear factor κB (NF-κB) inflammasome activation, decreased bone resorption, and improved bone quality, which were correlated with comparable and higher regulatory T cells (Treg) frequency in MI-2 and 12% RPS group, respectively. CONCLUSIONS: These findings suggested that the diet with 12% RPS could alleviate E. coli-induced bone loss in meat ducks by changing the gut microbial composition and promoting concomitant SCFAs production, and consequently inhibiting Malt1/NF-κB inflammasome activation and Treg cells expansion.
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The kynurenine pathway storm in epilepsy: mechanisms and therapeutic implications.
The kynurenine pathway (KP) is the main route for tryptophan (TRP) degradation and plays a crucial role in neuroinflammation, oxidative stress and neurotransmission, which holds significant clinical significance. The dysregulation of this pathway is closely related to neurological disorders such as epilepsy, and its metabolic products can promote the occurrence of epileptic seizures and comorbid depression. This review aims to clarify the complex mechanisms of the KP in the occurrence and development of epilepsy and to explore its potential as a therapeutic target for epilepsy and comorbid depression. This is a narrative review and synthesis of the current literature. We reviewed animal experiments and clinical studies, elaborating in detail on how metabolites of the KP and their key enzymes function in the context of epilepsy by regulating neuroinflammation, oxidative stress, glutamatergic signaling, and the gut-brain axis. We also explored the interaction between antiseizure medications (ASMs) and the KP, and evaluated the potential value of targeting key enzymes (such as indoleamine 2,3-dioxygenase, IDO) as a new therapeutic strategy for epilepsy. This review particularly focuses on the promoting effect of KP imbalance on comorbid depression, clarifying how IDO-mediated TRP metabolism changes constitute a common mechanism basis, jointly leading to the occurrence of epilepsy and depression-like behaviors. The occurrence and development of epilepsy are closely related to the imbalance of the KP, specifically manifested as a decrease in kynurenic acid (KYNA) level and an increase in quinolinic acid (QA) level. The IDO-mediated shift of TRP metabolism towards the KP is established as a critical mechanism underlying depression comorbidity in epilepsy. Therapeutic modulation of this pathway, through targeting key enzymes like IDO and restoring the KYNA/QA balance, presents a viable strategy for improving the cerebral microenvironment. This approach holds promise for enhancing seizure control, counteracting drug resistance, and concurrently alleviating comorbid depressive symptoms.
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Responses of broiler chickens to Eimeria challenge when fed a nucleotide-rich yeast extract.
Nucleotide-rich yeast extract (YN) was investigated for effects on growth performance, jejunal physiology, and cecal microbial activity in Eimeria-challenged broiler chickens. A total of 360-day-old male chicks (Ross × Ross 708) were placed on floor pens and provided a corn-soybean meal-based diet without or with YN (500 g/MT; n = 12). On d 10, 6 replicates per diet were orally administered with 1 mL of E. acervulina and E. maxima sporulated oocysts and the rest (non-challenged control) were administered with 1 mL of distilled water. On d 15, 5 birds/pen were then necropsied for intestinal lesion scores, histomorphology and cecal digesta pH, short chain fatty acids (SCFA), and microbial community using Illumina Miseq platform. Supplemental YN improved (P = 0.01) Feed conversion ratio (FCR) during the prechallenge phase (d 0 to 10). In the postchallenge period (d 11 to 15), Eimeria depressed (P < 0.05) Body weight gain (BWG) relative to non-challenged birds, whereas YN-fed birds had a higher (P = 0.05) BWG compared to that of non-YN-fed birds. There was an interaction between YN and Eimeria on jejunal villi height (VH) (P = 0.001) and expression of cationic amino acid transporter 1(CAT1) (P = 0.04). Specifically, in the absence of Eimeria, YN-fed birds had a shorter VH (892 vs. 1,020 μm) relative to that of control but longer VH (533 vs. 447 μm) in the presence of Eimeria. With respect to CAT1, YN-fed birds had a higher (1.65 vs. 0.78) expression when subjected to Eimeria than when not challenged. Independently, Eimeria decreased (P < 0.01) the jejunal expression of maltase, Na glucose transporter 1 and occludin genes, ceca digesta abundance of genus Clostridium cluster XlVa and Oscillibacter but increased (P < 0.01) jejunal proliferating cell nuclear antigen and interleukin 10. Interaction between YN and Eimeria was observed for ceca digesta pH (P = 0.04) and total SCFA (P = 0.01) such that YN increased SCFA in the absence of Eimeria but reduced SCFA and increased pH in the presence of Eimeria. In summary, Eimeria impaired performance and gut function and shifted gut microbiome; YN improved performance independently, attenuated Eimeria damage on indices of gut function, and modulated cecal microbiome.
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Differences in the individual curative effect of acupuncture for obese women with polycystic ovary syndrome based on metagenomic analysis: study protocol for a randomized controlled trial.
BACKGROUND: Polycystic ovary syndrome is a common cause of infertility and shows a high incidence in women of reproductive age. Acupuncture is an appropriate adjunctive treatment for PCOS. However, the add-on effect of acupuncture as an adjunctive treatment for obese women with PCOS has not been studied, and previous studies indicate that there are individual differences in the curative effect of acupuncture, while deeper research on the mechanism of differences in the individual curative effect of acupuncture for obese women with PCOS is still lacking. This trial aims to assess the add-on treatment efficacy of acupuncture for obese women with PCOS and to explore the role of the gut microbiome on the differences in the individual curative effect of acupuncture based on metagenomic analysis. METHODS/DESIGN: This is an open-label, randomized, controlled trial. A total of 86 obese women with PCOS will be recruited. Subjects will be randomly assigned to a study group and a control group in a 1:1 ratio, with 43 subjects in each group (10 patients from each group who meet the study criteria will participate in the metagenomic analysis). An additional 10 subjects who meet the study criteria will be recruited to a healthy control group. The study group will receive acupuncture and clomiphene citrate treatment; the control group will only receive clomiphene citrate. Acupuncture treatment will be conducted three times a week from the fifth day of menstruation or withdrawal bleeding until the start of the next menstruation, for up to three menstrual cycles. The primary outcome will be LH/FSH. The secondary outcomes will comprise biometric features, hormone biomarkers, metabolic biomarkers, inflammatory biomarkers, Self-Rating Anxiety Scale, Self-Rating Depression Scale, and metagenomic analysis. The outcomes will be measured at baseline and post-intervention. Data will be analyzed using SPSS 19.0, and the gut microbiome will be analyzed using metagenomic analysis. DISCUSSION: In this study, we are evaluating the add-on effects of acupuncture and exploring the mechanism of the differences in the individual curative effect of acupuncture based on the gut microbiome, which may provide evidence to explain the different outcomes of different trials on acupuncture for PCOS and hopefully to provide a new aspect to study the mechanism of acupuncture's treatment effect. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR2000029882 . Registered on 16 February 2020.
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Rifaximin modulates TRH and TRH-like peptide expression throughout the brain and peripheral tissues of male rats.
BACKGROUND: The TRH/TRH-R1 receptor signaling pathway within the neurons of the dorsal vagal complex is an important mediator of the brain-gut axis. Mental health and protection from a variety of neuropathologies, such as autism, Attention Deficit Hyperactivity Disorder, Alzheimer's and Parkinson's disease, major depression, migraine and epilepsy are influenced by the gut microbiome and is mediated by the vagus nerve. The antibiotic rifaximin (RF) does not cross the gut-blood barrier. It changes the composition of the gut microbiome resulting in therapeutic benefits for traveler's diarrhea, hepatic encephalopathy, and prostatitis. TRH and TRH-like peptides, with the structure pGlu-X-Pro-NH2, where "X" can be any amino acid residue, have reproduction-enhancing, caloric-restriction-like, anti-aging, pancreatic-β cell-, cardiovascular-, and neuroprotective effects. TRH and TRH-like peptides occur not only throughout the CNS but also in peripheral tissues. To elucidate the involvement of TRH-like peptides in brain-gut-reproductive system interactions 16 male Sprague-Dawley rats, 203 ± 6 g, were divided into 4 groups (n = 4/group): the control (CON) group remained on ad libitum Purina rodent chow and water for 10 days until decapitation, acute (AC) group receiving 150 mg RF/kg powdered rodent chow for 24 h providing 150 mg RF/kg body weight for 200 g rats, chronic (CHR) animals receiving RF for 10 days; withdrawal (WD) rats receiving RF for 8 days and then normal chow for 2 days. RESULTS: Significant changes in the levels of TRH and TRH-like peptides occurred throughout the brain and peripheral tissues in response to RF. The number of significant changes in TRH and TRH-like peptide levels in brain resulting from RF treatment, in descending order were: medulla (16), piriform cortex (8), nucleus accumbens (7), frontal cortex (5), striatum (3), amygdala (3), entorhinal cortex (3), anterior (2), and posterior cingulate (2), hippocampus (1), hypothalamus (0) and cerebellum (0). The corresponding ranking for peripheral tissues were: prostate (6), adrenals (4), pancreas (3), liver (2), testis (1), heart (0). CONCLUSIONS: The sensitivity of TRH and TRH-like peptide expression to RF treatment, particularly in the medulla oblongata and prostate, is consistent with the participation of these peptides in the therapeutic effects of RF.
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Integrative oncology in colorectal cancer: evidence-based strategies from prevention through survivorship.
Colorectal cancer (CRC) is a leading global malignancy, with approximately 1.9 million new cases and over 900,000 deaths recorded in 2022, yet evidence-based integrative oncology strategies remain inconsistently incorporated into routine care. This narrative review synthesizes current evidence across the full CRC care continuum, from primary prevention through long-term survivorship. High-fiber diets, Mediterranean dietary patterns, calcium supplementation, regular physical activity, healthy weight maintenance, and berberine each demonstrate reproducible CRC risk reduction in large prospective cohorts and multicenter randomized controlled trials. The CHALLENGE trial (NEJM 2025) provides the first randomized phase 3 evidence that structured exercise after adjuvant chemotherapy reduces disease recurrence (HR 0.72) and death (HR 0.63) in colon cancer. Aspirin chemoprevention requires individualized risk-benefit assessment per 2022 US Preventive Services Task Force guidelines; preliminary CaPP3 trial data (conference presentation, June 2025; not yet peer-reviewed) suggest non-inferiority of low-dose aspirin (75-100 mg/day) to 600 mg/day in Lynch syndrome, pending formal publication. Fusobacterium nucleatum promotes colorectal carcinogenesis through five mechanistically distinct pathways: FadA-mediated Wnt/β-catenin activation, Fap2- and CbpF-mediated immune evasion via TIGIT and CEACAM1, succinate-HIF-1α-EZH2-mediated immune suppression, Hippo pathway-mediated suppression of pyroptosis, and autophagy-induced chemoresistance. Perioperative multi-strain probiotics significantly reduce postoperative infectious complications, and fecal microbiota transplantation shows preliminary promise for sensitizing microsatellite-stable CRC to immunotherapy. The 2022-2024 SIO-ASCO and ASCO-SIO clinical practice guidelines endorse mindfulness-based interventions, yoga, and acupuncture for anxiety, depression, fatigue, and cancer-related pain. Systematic integration of these interventions into multidisciplinary CRC care requires standardized implementation frameworks, CRC-specific clinical trials for mind-body modalities, and bioavailability-optimized phytochemical formulations.
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Gut microbiome in schizophrenia and antipsychotic-induced metabolic alterations: a scoping review.
Schizophrenia (SCZ) is a severe mental disorder with high morbidity and lifetime disability rates. Patients with SCZ have a higher risk of developing metabolic comorbidities such as obesity and diabetes mellitus, leading to increased mortality. Antipsychotics (APs), which are the mainstay in the treatment of SCZ, increase the risk of these metabolic perturbations. Despite extensive research, the mechanism underlying SCZ pathophysiology and associated metabolic comorbidities remains unclear. In recent years, gut microbiota (GMB) has been regarded as a 'chamber of secrets', particularly in the context of severe mental illnesses such as SCZ, depression, and bipolar disorder. In this scoping review, we aimed to investigate the underlying role of GMB in the pathophysiology of SCZ and metabolic alterations associated with APs. Furthermore, we also explored the therapeutic benefits of prebiotic and probiotic formulations in managing SCZ and AP-induced metabolic alterations. A systematic literature search yielded 46 studies from both preclinical and clinical settings that met inclusion criteria for qualitative synthesis. Preliminary evidence from preclinical and clinical studies indicates that GMB composition changes are associated with SCZ pathogenesis and AP-induced metabolic perturbations. Fecal microbiota transplantation from SCZ patients to mice has been shown to induce SCZ-like behavioral phenotypes, further supporting the plausible role of GMB in SCZ pathogenesis. This scoping review recapitulates the preclinical and clinical evidence suggesting the role of GMB in SCZ symptomatology and metabolic adverse effects associated with APs. Moreover, this scoping review also discusses the therapeutic potentials of prebiotic/probiotic formulations in improving SCZ symptoms and attenuating metabolic alterations related to APs.