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Elevated Depressive Symptoms Shape Gut Barrier Integrity, LPS Translocation, and PUFA Composition in IBS-D: Evidence from a Low-FODMAP Dietary Intervention.
Introduction: Alterations of the microbiota-gut-brain axis, including increased intestinal permeability (IP), changes in microbial activity, and immune activation, are central to the pathophysiology of irritable bowel syndrome with diarrhea (IBS-D). The low-fermentable oligo-di-monosaccharides and polyols (FODMAP) diet (LFD) is an established therapy for IBS, yet its systemic effects, particularly in patients with elevated depressive symptoms, remain incompletely characterized. Methods: This single-arm pre-post study investigated associations between depressive symptom severity and markers of small IP (s-IP), endotoxin exposure, inflammation, and erythrocyte membrane polyunsaturated fatty acid (PUFA) composition in 43 IBS-D patients undergoing a 12-week personalized LFD. Patients were classified using the Symptom Checklist-90-Revised depression subscale into those with (d+, n = 23) and without (d-, n = 20) clinically elevated depressive symptoms. Results: At baseline, d+ patients exhibited higher s-IP, circulating lipopolysaccharide levels, inflammatory markers, and a more pro-inflammatory PUFA profile. Following LFD, significant improvements in symptoms and several biological parameters were observed in the overall cohort. Greater absolute changes in d+ patients were consistent with their higher baseline values rather than indicating differential responsiveness. Baseline depressive symptoms were not significantly associated with the magnitude of post-intervention changes in IP or inflammatory markers. Conclusions: These findings suggest that elevated depressive symptoms identify an IBS-D subgroup characterized by greater baseline biological burden. Results should be interpreted as associative given the single-arm design, absence of a control group, and the concurrent reduction in body weight, which may have influenced the observed changes. Randomized controlled studies are needed to clarify the role of dietary interventions in modulating gut-brain axis-related pathways in IBS-D.
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The Role of Gut Microbiota, Nutrition, and Physical Activity in Depression and Obesity-Interdependent Mechanisms/Co-Occurrence.
Obesity and depression are interdependent pathological disorders with strong inflammatory effects commonly found worldwide. They determine the health status of the population and cause key problems in terms of morbidity and mortality. The role of gut microbiota and its composition in the treatment of obesity and psychological factors is increasingly emphasized. Published research suggests that prebiotic, probiotic, or symbiotic preparations can effectively intervene in obesity treatment and mood-dysregulation alleviation. Thus, this literature review aims to highlight the role of intestinal microbiota in treating depression and obesity. An additional purpose is to indicate probiotics, including psychobiotics and prebiotics, potentially beneficial in supporting the treatment of these two diseases.
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The complex interplay between psoriasis and depression: from molecular mechanisms to holistic treatment approaches.
Psoriasis is an inflammatory disease driven by immune dysregulation. Numerous epidemiological studies have confirmed a significant association between psoriasis and mental health disorders, particularly depression. Recent research has increasingly underscored the common pathogenic mechanisms between psoriasis and depression. The release of factors such as TNF, IL-6, and IL-8 not only directly drives abnormal proliferation of skin keratinocytes and immune infiltration but also disrupts the blood-brain barrier, inducing neuroinflammation. Hypothalamic-pituitary-adrenal (HPA) axis dysfunction leads to inflammation amplification. Additionally, microbiota dysbiosis-such as a reduced abundance of Actinobacteria and Firmicutes-decreases the production of short-chain fatty acids and increases the absorption of lipopolysaccharides into the bloodstream via the "gut-brain-skin axis," thereby exacerbating systemic and neuroinflammatory conditions. Based on this understanding, clinical practice demands an integrated "biological-psychological-social" approach. Biologics (e.g., adalimumab, secukinumab, and guselkumab) can simultaneously ameliorate skin lesions and depressive symptoms. When combined with psychological interventions-including cognitive behavioral therapy and mindfulness therapy-a multidisciplinary collaboration involving dermatology, rheumatology, and psychology is essential to formulate a tailored treatment plan. This review systematically outlines the core mechanisms underlying comorbidity of these two diseases, as well as multidimensional treatment strategies.
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Gastrointestinal Issues in Depression, Anxiety, and Neurodegenerative Diseases: A Systematic Review on Pathways and Clinical Targets Implications.
INTRODUCTION: Multiple illnesses commonly involve both the Central Nervous System (CNS) and the Gastrointestinal Tract (GI) simultaneously. Consistent evidence suggests that neurological disorders impair GI tract function and worsen the symptomatology and pathophysiology of digestive disorders. On the other hand, it has been proposed that early functional changes in the GI tract contribute to the genesis of several CNS illnesses. Additionally, the role played by the gut in these diseases can be seen as a paradigm for how the gut and the brain interact. METHODS: We mentioned significant GI symptoms and discussed how the GI tract affects central nervous system illnesses, including depression, anxiety, Alzheimer's disease, and Parkinson's disease in this study. We also explored potential pathophysiological underpinnings and novel targets for the creation of future therapies targeted at gut-brain connections. RESULTS & DISCUSSION: In this situation, modulating the gut microbiota through the administration of fecal microbiota transplants or probiotics may represent a new therapeutic option for this population, not only to treat GI problems but also behavioral problems, given the role that dysbiosis and leaky gut play in many neurological disorders. CONCLUSION: Accurate diagnosis and treatment of co-existing illnesses also require coordination between psychiatrists, neurologists, gastroenterologists, and other specialties, as well as a thorough history and thorough physical examination.
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Deciphering the gut microbiota's (Coprococcus and Subdoligranulum) impact on depression: Network pharmacology and molecular dynamics simulation.
Depression, a prevalent mental health condition, significantly impacts global mental impairment rates. While antidepressants are commonly used, treatment-resistant depression (TRD) poses a challenge. Emerging research highlights the role of the gut microbiota in depression through the gut-brain axis. This study identifies key genes associated with depression influenced by specific gut microbiota, Coprococcus and Subdoligranulum. Using bioinformatics tools, potential targets were elucidated, and molecular docking studies were performed. Furthermore, gene expression analysis identified hub-genes related to depression, intersecting with metabolite targets. Protein-protein interaction analysis revealed pivotal targets such as PTGS2 and MMP9. Molecular docking demonstrated 3-Indolepropionic acid's superior affinity over (R)-3-(4-Hydroxyphenyl)lactate. Physicochemical properties and toxicity profiles were compared, suggesting favorable attributes for 3-Indolepropionic acid. Molecular dynamics simulations confirmed stability and interactions of compounds with target proteins. This comprehensive approach sheds light on the complex interplay between gut microbiota, genes, and depression, emphasizing the potential for microbiota-targeted interventions in mental health management.
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Feeding melancholic microbes: MyNewGut recommendations on diet and mood.
Depression is a highly prevalent disorder which exerts a major economic impact in all European countries. The brain-gut-microbiota axis has been described as a new paradigm for advancing understanding and treatment of the disorder. There is now over-whelming evidence to support the fact that gut microbes have a major impact on central neurochemistry and behaviour, especially stress related disorders such as depression. Recent studies indicate that patients with depression have a gut dysbiosis. The reason for this dysbiosis is uncertain. Over recent decades, dietary patterns in Europe and elsewhere have undergone major compositional changes, with increased intakes of red meat, high fat foods, and refined sugars. Individuals who consume a Mediterranean diet have lower rates of depression and a recent study suggests that a Mediterranean diet may have antidepressant properties. Assuming this to be the case, which components of the Mediterranean diet mediate the effects? Highly levels of polyphenols or polyunsaturated fatty acids are obvious candidates. We in the MyNewGut consortium recommend that patients with depression or vulnerability to depression should be encouraged to enhance a plant-based diet with a high content of grains/fibres and fish.
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Multiple Sclerosis, Gut Microbiota and Permeability: Role of Tryptophan Catabolites, Depression and the Driving Down of Local Melatonin.
BACKGROUND: Alterations in gut microbiota, coupled to increased gut permeability are now widely recognized as having a role in the etiology, course and treatment of many medical conditions, including autoimmune and neurodegenerative disorders. METHODS: In this review, the role that such gut changes play over the course of multiple sclerosis (MS) is detailed. RESULTS: Given the wide array of biological factors and processes that have been shown to be altered in MS, including changes in the gut, this allows for a better integration of the diverse array of pathophysiological processes linked to MS. Such pathophysiological processes include increases in oxidative and nitrosative stress, pro-inflammatory immune responses, especially T helper (Th)17 cell proliferation and activation, tryptophan catabolites, pain, fatigue and increased levels of depression. By raising levels of immune activation, increased gut permeability and alterations in gut microbiota impact on all of these MS-associated processes. Alterations in the regulation of local melatonergic pathway activation is proposed to be an important hub for such pathophysiological processes in MS, allowing for the increased frequency of depression that may be prodromal in MS, both in the first episode as well as in relapses, to become more intimately associated with the etiology and course of MS. We propose this occurs by decreasing serotonin availability as a precursor for the melatoninergic pathways. CONCLUSION: Changes in the gut are evident in the early stages of MS, including in paediatric MS, and may interact with pro-inflammatory genetic susceptibility genes to drive the biological underpinnings of MS. Such a conceptualization of the biological underpinnings of MS also has treatment implications.
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Unravelling the antimicrobial action of antidepressants on gut commensal microbes.
Over the past decade, there has been increasing evidence highlighting the implication of the gut microbiota in a variety of brain disorders such as depression, anxiety, and schizophrenia. Studies have shown that depression affects the stability of gut microbiota, but the impact of antidepressant treatments on microbiota structure and metabolism remains underexplored. In this study, we investigated the in vitro antimicrobial activity of antidepressants from different therapeutic classes against representative strains of human gut microbiota. Six different antidepressants: phenelzine, venlafaxine, desipramine, bupropion, aripiprazole and (S)-citalopram have been tested for their antimicrobial activity against 12 commensal bacterial strains using agar well diffusion, microbroth dilution method, and colony counting. The data revealed an important antimicrobial activity (bacteriostatic or bactericidal) of different antidepressants against the tested strains, with desipramine and aripiprazole being the most inhibitory. Strains affiliating to most dominant phyla of human microbiota such as Akkermansia muciniphila, Bifidobacterium animalis and Bacteroides fragilis were significantly altered, with minimum inhibitory concentrations (MICs) ranged from 75 to 800 μg/mL. A significant reduction in bacterial viability was observed, reaching 5 logs cycle reductions with tested MICs ranged from 400 to 600 μg/mL. Our findings demonstrate that gut microbiota could be altered in response to antidepressant drugs.
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The Effect and Mechanism of Exercise Training on Rats with Poststroke Depression Based on the Intestinal Flora.
Depression of poststroke depression (PSD) is the most common neuropsychiatric complication after stroke. Patients with PSD had higher mortality, more cognitive disorder, lower quality of life, and higher suicidal tendency. The pathogenesis of PSD mainly involves neurotransmitter inflammatory factors, HPA and BDNF. Enteral dysfunction and intestinal flora disorders caused by stroke can participate in the pathogenesis of PSD through various ways, such as immune, endocrine, and nervous system. In this experiment, we used exercise training as an intervention means to explore the curative effect and possible mechanism by observing the changes of behavior, inflammatory factors, and intestinal flora in rats. The results show that the mechanism of exercise training to improve the depressive behavior of rats may be related to inhibiting the expression of proinflammatory factors and increasing the number of lactic acid bacteria in the intestine.
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Gut-derived systemic inflammation as a driver of depression in chronic liver disease.
Depression and chronic liver disease (CLD) are important causes of disability, morbidity and mortality worldwide and their prevalence continues to rise. The rate of depression in CLD is high compared to that of the general population and is comparable to the increased rates observed in other medical comorbidities and chronic inflammatory conditions. Notably, a comorbid diagnosis of depression has a detrimental effect on outcomes in cirrhosis. Systemic inflammation is pivotal in cirrhosis-associated immune dysfunction - a phenomenon present in advanced CLD (cirrhosis) and implicated in the development of complications, organ failure, disease progression, increased infection rates and poor outcome. The presence of systemic inflammation is also well-documented in a cohort of patients with depression; peripheral cytokine signals can result in neuroinflammation, behavioural change and depressive symptoms via neural mechanisms, cerebral endothelial cell and circumventricular organ signalling, and peripheral immune cell-to-brain signalling. Gut dysbiosis has been observed in both patients with cirrhosis and depression. It leads to intestinal barrier dysfunction resulting in increased bacterial translocation, in turn activating circulating immune cells, leading to cytokine production and systemic inflammation. A perturbed gut-liver-brain axis may therefore explain the high rates of depression in patients with cirrhosis. The underlying mechanisms explaining the critical relationship between depression and cirrhosis remain to be fully elucidated. Several other psychosocial and biological factors are likely to be involved, and therefore the cause is probably multifactorial. However, the role of the dysfunctional gut-liver-brain axis as a driver of gut-derived systemic inflammation requires further exploration and consideration as a target for the treatment of depression in patients with cirrhosis.