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Irritable Bowel Syndrome and Stress-Related Psychiatric Co-morbidities: Focus on Early Life Stress.
Irritable bowel syndrome is a functional gastrointestinal disorder, with stress playing a major role in onset and exacerbation of symptoms such as abdominal pain and altered bowel movements. Stress-related disorders including anxiety and depression often precede the development of irritable bowel syndrome and vice versa. Stressor exposure during early life has the potential to increase an individual's susceptibility to both irritable bowel syndrome and psychiatric disease indicating that there may be a common origin for these disorders. Moreover, adverse early life events significantly impact upon many of the communication pathways within the brain-gut-microbiota axis, which allows bidirectional interaction between the central nervous system and the gastrointestinal tract. This axis is proposed to be perturbed in irritable bowel syndrome and studies now indicate that dysfunction of this axis is also seen in psychiatric disease. Here we review the co-morbidity of irritable bowel syndrome and psychiatric disease with their common origin in mind in relation to the impact of early life stress on the developing brain-gut-microbiota axis. We also discuss the therapeutic potential of targeting this axis in these diseases.
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Pharmacological restoration of gut barrier function in stressed neonates partially reverses long-term alterations associated with maternal separation.
RATIONALE: Intestinal permeability plays an important role in gut-brain axis communication. Recent studies indicate that intestinal permeability increases in neonate pups during maternal separation (MS). OBJECTIVES: The present study aims to determine whether pharmacological inhibition of myosin light chain kinase (MLCK), which regulates tight junction contraction and controls intestinal permeability, in stressed neonates, protects against the long-term effects of MS. METHODS: Male Wistar rats were exposed to MS (3 h per day from post-natal day (PND)2 to PND14) or left undisturbed and received daily intraperitoneal injection of a MLCK inhibitor (ML-7, 5 mg/kg) or vehicle during the same period. At adulthood, emotional behaviors, corticosterone response to stress, and gut microbiota composition were analyzed. RESULTS: ML-7 restored gut barrier function in MS rats specifically during the neonatal period. Remarkably, ML-7 prevented MS-induced sexual reward-seeking impairment and reversed the alteration of corticosterone response to stress at adulthood. The effects of ML-7 were accompanied by the normalization of the abundance of members of Lachnospiraceae, Clostridiales, Desulfovibrio, Bacteroidales, Enterorhabdus, and Bifidobacterium in the feces of MS rats at adulthood. CONCLUSIONS: Altogether, our work suggests that improvement of intestinal barrier defects during development may alleviate some of the long-term effects of early-life stress and provides new insight on brain-gut axis communication in a context of stress.
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"Indole-gence" for the mind.
Surging depression rates highlight the need for innovative strategies beyond the traditional focus on the brain. In this issue of Cell Host & Microbe, Cheng et al. uncover a role for the gut microbiota in depression through the intestinal receptor Grp35 and indole pathway, offering hope in fighting against depression.
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Diabesity and mood disorders: Multiple links through the microbiota-gut-brain axis.
The global prevalence of diabesity is on the rise, and the clinical, social and economic health burden arising from this epidemic is aggravated by a significant co-morbidity of diabesity with neuropsychiatric disease, particularly depression. Importantly, not only is the prevalence of mood disorders elevated in patients with type 2 diabetes, depressed patients are also more prone to develop diabetes. This reciprocal relationship calls for a molecular and systemic analysis of diabesity-brain interactions to guide preventive and therapeutic strategies. The analysis we are presenting in this review is modelled on the microbiota-gut-brain axis, which provides the brain with information from the gut not only via the nervous system, but also via a continuous stream of microbial, endocrine, metabolic and immune messages. This communication network offers important clues as to how obesity and diabetes could target the brain to provoke neuropsychiatric disease. There is emerging evidence that the gut microbiota is orchestrating a multiplicity of bodily functions that are intimately related to the immune, metabolic and nervous systems and that gut dysbiosis spoils the homeostasis between these systems. In our article we highlight two groups of molecular links that seem to have a significant bearing on the impact of diabesity on the brain. On the one hand, we focus on microbiota-related metabolites such as short-chain fatty acids, tryptophan metabolites, immune stimulants and endocannabinoids that are likely to play a mediator role. On the other hand, we discuss signalling molecules that operate primarily in the brain, specifically neuropeptide Y, brain-derived neurotrophic factor and γ-amino butyric acid, that are disturbed by microbial factors, obesity and diabetes and are relevant to mental illness. Finally, we address the usefulness of diet-related interventions to suspend the deleterious relationship between diabesity and mood disorders.
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Novel aspects of enteric serotonergic signaling in health and brain-gut disease.
Gastrointestinal (GI) comorbidities are common in individuals with mood and behavioral dysfunction. Similarly, patients with GI problems more commonly suffer from co-morbid psychiatric diagnoses. Although the central and enteric nervous systems (CNS and ENS, respectively) have largely been studied separately, there is emerging interest in factors that may contribute to disease states involving both systems. There is strong evidence to suggest that serotonin may be an important contributor to these brain-gut conditions. Serotonin has long been recognized for its critical functions in CNS development and function. The majority of the body's serotonin, however, is produced in the GI tract, where it plays key roles in ENS development and function. Further understanding of the specific impact that enteric serotonin has on brain-gut disease may lay the foundation for the creation of novel therapeutic targets. This review summarizes the current data focusing on the important roles that serotonin plays in ENS development and motility, with a focus on novel aspects of serotonergic signaling in medical conditions in which CNS and ENS co-morbidities are common, including autism spectrum disorders and depression.
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Microbiota alterations are related to migraine food triggers and inflammatory markers in chronic migraine patients with medication overuse headache.
OBJECTIVE: Chronic migraine (CM) patients with medication overuse headache (MOH) were recently shown to be associated with leaky gut and inflammation. We aimed to investigate gut microbiota profiles of CM patients with MOH, and their correlations with inflammatory serum parameters, migraine food triggers, and comorbid anxiety and depression. MATERIALS AND METHODS: The study included women participants (32 CM patients with NSAID overuse headache, and 16 healthy non-headache sufferers). Migraine duration, monthly migraine headache days, presence of irritable bowel syndrome symptoms, and HADS-D and HADS-A scores were recorded. Serum samples were collected to measure circulating LPS, HMGB1, HIF-1α, and IL-6. The gut microbiota profiles of the patients were evaluated using fecal samples. RESULTS: Serum LPS, HMGB1, HIF-1α, and IL-6 levels were significantly higher in the CM + MOH group compared to the healthy controls. HADS-A and HADS-D scores were considerably higher in the CM + MOH group compared to the healthy controls. In the microbiota analysis, alpha and beta diversities were similar between the two groups. The class Clostridia, the order Eubacteriales, and the genus Ruminococcus were less abundant in the CM + NSAID overuse headache group compared to the control group. At the genus level Desulfovibrio, Gemmiger, and Dialister and at the species level, Clostridium fessum, Blautia luti, Dorea longicatena, Eubacterium coprostanoligenes, and Gemmiger formicilis were more abundant in the CM + NSAID overuse headache group compared to the control group. Desulfovibrio, Gemmiger, Dialister, Ethanoligenens harbinense, Eubacterium coprostanoligenes, Dorea longicatena, and Thermoclostridium stercorarium showed positive correlations and Clostridia bacteria showed negative correlations with migraine food triggers. Positive correlations were found between LPS and Hapalosiphonaceae, HMGB1 and Melghirimyces, HIF1-α and Rouxeilla and Blautia luti, IL-6 and Melghirimyces and Ruminococcus. CONCLUSION: In CM patients with MOH, we have revealed the presence of dysbiosis towards an inflammatory state, and positive correlations were shown between altered gut microbiota and inflammatory serum parameters and migraine food triggers.
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Current evidence linking diet to gut microbiota and brain development and function.
The gut:brain axis is emerging as an important information highway linking the foods we eat with neurophysiological development and functions. Some gut microorganisms have shown to alleviate anxiety and depression, improve cognitive performance and play a role in brain development in early life. However, most studies were conducted in laboratory animals and these findings await confirmation in carefully designed human interventions. Similarly, little attention has been given to how diet:microbe interactions within the gut can impact on neurotransmitter production or their subsequent biological effects within the nervous system. In this review, we discuss the possible influence of carbohydrates, polyphenols, lipids and proteins colonic fermentation on production, bioavailability and biological activity of metabolites linked to the gut-microbiota-brain axis. An increased understanding of how nervous system may be regulated by diet will greatly enhance our ability to design dietary strategies to improve healthy brain development and functions.
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Advances in the study of the relationship between gut microbiota and erectile dysfunction.
INTRODUCTION: In recent years, in-depth research has revealed that gut microbiota has an inseparable relationship with erectile dysfunction (ED) in men. OBJECTIVES: (1) To review the correlation between gut microbiota and ED from the perspective of its impact on men's mental health, metabolism, immunity, and endocrine regulation and (2) to provide reference to further explore the pathogenesis of ED and the improvement of clinical treatment plans. METHODS: PubMed was used for the literature search to identify publications related to ED and gut microbiota. RESULTS: Gut microbiota may induce depression and anxiety through the microbiota-gut-brain axis, leading to the occurrence of psychological ED. It may also cause vascular endothelial dysfunction and androgen metabolism disorder by interfering with lipid metabolism, immunity, and endocrine regulation, leading to the occurrence of organic ED. CONCLUSION: Gut microbiota and its metabolites play an important role in the occurrence and development of ED. As a new influencing factor of ED, gut microbiota disorder is expected to become a target for treatment.
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Microbiota-gut-brain signalling in Parkinson's disease: Implications for non-motor symptoms.
Parkinson's disease is the second most common neurodegenerative disorder, affecting 1-2% of the population over 65 years of age. The primary neuropathology is the loss of midbrain dopaminergic neurons, resulting in characteristic motor deficits, upon which the clinical diagnosis is based. However, a number of significant non-motor symptoms (NMS) are also evident that appear to have a greater impact on the quality of life of these patients. In recent years, it has become increasingly apparent that neurobiological processes can be modified by the bi-directional communication that occurs along the brain-gut axis. The microbiota plays a key role in this communication throughout different routes in both physiological and pathological conditions. Thus, there has been an increasing interest in investigating how microbiota changes within the gastrointestinal tract may be implicated in health and disease including PD. Interestingly α-synuclein-aggregates, the cardinal neuropathological feature in PD, are present in both the submucosal and myenteric plexuses of the enteric nervous system, prior to their appearance in the brain, indicating a possible gut to brain route of "prion-like" spread. In this review we highlight the potential importance of gut to brain signalling in PD with particular focus on the role of the microbiota as major player in this communication.
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The correlation between intestinal dysbiosis and the development of ankylosing spondylitis.
The pathogenesis and development of ankylosing spondylitis (AS) is concealed and complicated. In recent years, alterations in gut microbiota of AS patients have been largely investigated, although the underlying mechanisms remain unclear. This article reviews the recent studies on changes of gut microbiota in AS patients, and discusses the possible correlation between intestinal dysbiosis and AS development from aspects including genetic factor HLA-B27, mucosal immune responses and the depression accompanying AS.