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The Effects of Physical Activity on the Gut Microbiota and the Gut-Brain Axis in Preclinical and Human Models: A Narrative Review.
Increasing evidence supports the importance of the gut microbiota (GM) in regulating multiple functions related to host physical health and, more recently, through the gut-brain axis (GBA), mental health. Similarly, the literature on the impact of physical activity (PA), including exercise, on GM and GBA is growing. Therefore, this narrative review summarizes and critically appraises the existing literature that delves into the benefits or adverse effects produced by PA on physical and mental health status through modifications of the GM, highlighting differences and similarities between preclinical and human studies. The same exercise in animal models, whether performed voluntarily or forced, has different effects on the GM, just as, in humans, intense endurance exercise can have a negative influence. In humans and animals, only aerobic PA seems able to modify the composition of the GM, whereas cardiovascular fitness appears related to specific microbial taxa or metabolites that promote a state of physical health. The PA favors bacterial strains that can promote physical performance and that can induce beneficial changes in the brain. Currently, it seems useful to prioritize aerobic activities at a moderate and not prolonged intensity. There may be greater benefits if PA is undertaken from a young age and the effects on the GM seem to gradually disappear when the activity is stopped. The PA produces modifications in the GM that can mediate and induce mental health benefits.
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Gut microbiota-driven metabolites modulate the development of stress-related mental disorders.
Stress-related mental disorders, including depression, anxiety, and post-traumatic stress disorder, represent a major global health burden, yet their underlying biological mechanisms and effective therapeutic strategies remain incompletely understood. Growing evidence from both preclinical and clinical studies indicates that alterations in gut microbiota composition and function are closely associated with the onset and progression of these disorders. A central role of the gut microbiota is the biotransformation of dietary and host-derived substrates into diverse metabolites that enter systemic circulation and influence host physiology. In this review, we highlight gut microbiota-driven metabolites. short-chain fatty acids, amino acid-related metabolites, bile acids, and monoamine-related metabolites, as key mediators of gut-brain communication that influence neural, immune, epigenetic, and endocrine processes involved in stress-related mental disorders. We summarize emerging microbial and metabolic signatures identified in animal models and human studies. Furthermore, we discuss microbiome-targeted strategies for the prevention and treatment. However, the complexity of the gut microbiota and pronounced inter-individual variability limit causal inference from current clinical studies. Consequently, translating these findings into clinical practice will require standardized study designs, longitudinal clinical investigations, and the integration of multi-omics approaches to advance precision microbiome-based interventions for psychiatric disorders.
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Social anxiety disorder-associated gut microbiota increases social fear.
Social anxiety disorder (SAD) is a crippling psychiatric disorder characterized by intense fear or anxiety in social situations and their avoidance. However, the underlying biology of SAD is unclear and better treatments are needed. Recently, the gut microbiota has emerged as a key regulator of both brain and behaviour, especially those related to social function. Moreover, increasing data supports a role for immune function and oxytocin signalling in social responses. To investigate whether the gut microbiota plays a causal role in modulating behaviours relevant to SAD, we transplanted the microbiota from SAD patients, which was identified by 16S rRNA sequencing to be of a differential composition compared to healthy controls, to mice. Although the mice that received the SAD microbiota had normal behaviours across a battery of tests designed to assess depression and general anxiety-like behaviours, they had a specific heightened sensitivity to social fear, a model of SAD. This distinct heightened social fear response was coupled with changes in central and peripheral immune function and oxytocin expression in the bed nucleus of the stria terminalis. This work demonstrates an interkingdom basis for social fear responses and posits the microbiome as a potential therapeutic target for SAD.
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High-resolution metagenomic characterization of gut microbiota composition and functional pathways in irritable bowel syndrome.
Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder characterized by abdominal pain, altered bowel habits, and frequent comorbidity with anxiety and depression. The gut microbiota has been implicated in gut-brain axis (GBA) dysfunction, but consistent microbial signatures remain unclear. We performed whole metagenome shotgun sequencing of stool samples from 63 female patients with moderate to severe IBS and 34 female healthy controls and assessed microbial composition and functional pathways. Microbial richness and diversity were slightly reduced in IBS, though with high variability and no robust separation from controls. Differential abundance analyses revealed enrichment of Streptococcus sp. and the sulfate-reducing bacterium Desulfovibrio piger in IBS, alongside reductions in Bifidobacterium and Methanobrevibacter. Functional profiling identified 39 differentially abundant pathways: amino acid biosynthesis (e.g., L-isoleucine, L-threonine) was more prominent in IBS, while carbohydrate degradation pathways (e.g., galactose, stachyose) were enriched in healthy controls. These findings indicate modest but significant IBS-associated shifts in gut microbial composition and function that may contribute to IBS symptoms. However, high intra-group variability underscores the complexity of IBS and highlights the need for larger, multi-omics studies to define robust microbial markers. These results contribute to a growing body of evidence emphasizing the complexity of gut microbiota-host interactions and the need for high-resolution, systems-level approaches in microbiome-associated disorders.
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Stressed to the Core: Inflammation and Intestinal Permeability Link Stress-Related Gut Microbiota Shifts to Mental Health Outcomes.
Stress levels are surging, alongside the incidence of stress-related psychiatric disorders. Perhaps a related phenomenon, especially in urban areas, the human gut contains fewer bacterial species than ever before. Although the functional implications of this absence are unclear, one consequence may be reduced stress resilience. Preclinical and clinical evidence has shown how stress exposure can alter the gut microbiota and their metabolites, affecting host physiology. Also, stress-related shifts in the gut microbiota jeopardize tight junctions of the gut barrier. In this context, bacteria and bacterial products can translocate from the gut to the bloodstream, lymph nodes, and other organs, thereby modifying systemic inflammatory responses. Heightened circulating inflammation can be an etiological factor in stress-related psychiatric disorders, including some cases of depression. In this review, we detail preclinical and clinical evidence that traces these brain-to-gut-to-brain pathways that underlie stress-related psychiatric disorders and potentially affect their responsivity to conventional psychiatric medications. We also review evidence for interventions that modulate the gut microbiota (e.g., antibiotics, probiotics, prebiotics) to reduce stress responses and psychiatric symptoms. Lastly, we discuss challenges to translation and opportunities for innovations that could impact future psychiatric clinical practice.
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The role of the intestinal microbiome in cognitive decline in patients with kidney disease.
Cognitive decline is frequently seen in patients with chronic kidney disease (CKD). The causes of cognitive decline in these patients are likely to be multifactorial, including vascular disease, uraemic toxins, blood-brain barrier leakage, and metabolic and endocrine changes. Gut dysbiosis is common in patients with CKD and contributes to the increase in uraemic toxins. However, the gut microbiome modulates local and systemic levels of several metabolites such as short-chain fatty acids or derivatives of tryptophan metabolism, neurotransmitters, endocannabinoid-like mediators, bile acids, hormones such as glucagon-like peptide 1 (GLP1) or cholecystokinin (CCK). These factors can affect gut function, immunity, autonomic nervous system activity and various aspects of brain function. Key areas include blood-brain barrier integrity, nerve myelination and survival/proliferation, appetite, metabolism and thermoregulation, mood, anxiety and depression, stress and local inflammation. Alterations in the composition of the gut microbiota and the production of biologically active metabolites in patients with CKD are well documented and are favoured by low-fiber diets, elevated urea levels, sedentary lifestyles, slow stool transit times and polypharmacy. In turn, dysbiosis can modulate brain function and cognitive processes, as discussed in this review. Thus, the gut microbiome may contribute to alterations in cognition in patients with CKD and may be a target for therapeutic interventions using diet, prebiotics and probiotics.
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Understanding the Connection Between the Gut-Brain Axis and Stress/Anxiety Disorders.
PURPOSE OF REVIEW: We review the association of the microbiota-gut-brain axis and anxiety disorder or stress. RECENT FINDING: The microbiota-gut-brain axis mechanism encompasses a bidirectional relationship between the brain and gastrointestinal organs. Dysregulation of the microbiota-gut-brain axis has been actively revealed in the context of various psychiatric diseases such as neurodevelopmental disorders, schizophrenia, anxiety disorders, and depression. We suggest that onset of anxiety disorders may be correlated with activation of a microbiota-gut-brain mechanism involving the immune system, neurotransmitters, and the hormonal system. By applying a microbiota-gut-brain axis mechanism, the possibility of using gastrointestinal system drugs such as probiotics and antibiotics as treatments for anxiety disorders is a possibility. Although modification of the microbiota-gut-brain axis mechanism has yet to be adopted clinically, it is expected that novel strategies employing this mechanism will be developed and deployed as new treatments not only for anxiety disorders, but also other psychiatric diseases.
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Bacterial Extracellular Vesicles and the Gut-Microbiota Brain Axis: Emerging Roles in Communication and Potential as Therapeutics.
Bacterial extracellular vesicles (BEVs) have emerged as candidate signaling vectors for long-distance interkingdom communication within the gut-microbiota brain axis. Most bacteria release these nanosized vesicles, capable of signaling to the brain via their abundant protein and small RNA cargo, possibly directly via crossing the blood-brain barrier. BEVs have been shown to regulate brain gene expression and induce pathology at most stages of neuroinflammation and neurodegeneration, and thus they may play a causal role in diseases such as Alzheimer's, Parkinson's, and depression/anxiety. On the other hand, BEVs have intrinsic therapeutic properties that may be relevant to probiotic therapy and can also be engineered to function as drug delivery vehicles and vaccines. Thus, BEVs may be both a cause of and solution to neuropathological conditions. In this review, current knowledge of the physiological roles of BEVs as well as state of the art pertaining to the development of therapeutic BEVs in the context of the microbiome-gut-brain axis are summarized.
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Evolution of the Human Diet and Its Impact on Gut Microbiota, Immune Responses, and Brain Health.
The relatively rapid shift from consuming preagricultural wild foods for thousands of years, to consuming postindustrial semi-processed and ultra-processed foods endemic of the Western world less than 200 years ago did not allow for evolutionary adaptation of the commensal microbial species that inhabit the human gastrointestinal (GI) tract, and this has significantly impacted gut health. The human gut microbiota, the diverse and dynamic population of microbes, has been demonstrated to have extensive and important interactions with the digestive, immune, and nervous systems. Western diet-induced dysbiosis of the gut microbiota has been shown to negatively impact human digestive physiology, to have pathogenic effects on the immune system, and, in turn, cause exaggerated neuroinflammation. Given the tremendous amount of evidence linking neuroinflammation with neural dysfunction, it is no surprise that the Western diet has been implicated in the development of many diseases and disorders of the brain, including memory impairments, neurodegenerative disorders, and depression. In this review, we discuss each of these concepts to understand how what we eat can lead to cognitive and psychiatric diseases.
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[Functional disorders in chronic inflammatory bowel disease: the gut-brain axis].
BACKGROUND: In patients with inflammatory bowel diseases (IBD), functional complaints frequently persist after the clearing of inflammation and are clinically difficult to distinguish from symptoms of inflammation. In recent years, the influence of bidirectional communication between the gut and brain on gut physiology, emotions, and behavior has been demonstrated. RESEARCH QUESTIONS: What mechanisms underlie the development of functional gastrointestinal complaints in patients with irritable bowel syndrome (IBS) and IBD? What therapeutic approaches arise from this? MATERIALS AND METHODS: Narrative review. RESULTS: The pathogenesis of IBS involves interactions between psychosocial factors, genetics, and microbiota as well as the central and peripheral nervous systems. The interplay between stress and visceral hypersensitivity is of central importance. Therapeutically, lifestyle changes with stress reduction and exercise alongside dietary, pharmacological, and psychotherapeutic options are useful. DISCUSSION: The treatment of functional gastrointestinal disorders remains challenging, as pharmacological therapies are often ineffective and gut-directed psychotherapies are rarely available.