Браузер не даёт сохранять данные (например, приватный режим): закладки пропадут после закрытия вкладки.
Поиск статей PubMed
Ключевые слова, автор, журнал, годы — результаты из PubMed, аннотации с переводом на русский, закладки в браузере.
Найдено: 3 214
Страница 307 из 322-
The microbiome as a key regulator of brain, behavior and immunity: Commentary on the 2017 named series.
The focus on the microbiome for the 2017 Named Series in Brain, Behavior, and Immunity reflects the rapidly growing interest in commensal microbes and the effects that they can have on physiological processes often studied in PsychoNeuroImmunology Research. The studies included in this Named Series show that commensal microbes can impact immune system activity, as well as brain and behavioral processes across the lifespan, and are involved in behavioral and immunological responses to social stresses. The studies also show that dietary effects on brain, behavior, and immunity often involve alterations of the gut microbiota. Thus, diet can be used therapeutically for diseases and conditions involving the brain, behavior, and immunity, as can treatment with both pre- and probiotics. While this has been widely tested in animal models, fewer studies have focused on pre- and probiotic treatment in humans. The studies in this Named Series highlight the challenges of probiotic research in human populations, but also highlight the future promise of probiotics for human health. While emotional disorders, such as anxiety and depression have been often been linked to alterations in the gut microbiota, studies in this Named Series identify new domains involving interactions between the microbiota, brain, behavior, and immunity, including schizophrenia, traumatic brain injury, and stroke. As a whole, this collection of work demonstrates the importance of the microbiome in regulating key aspects of immunity, brain, and behavior, and provides important rationale for extending the work so that findings can be translated into clinical practice.
-
Associations of body fat percentage-based obesity with depression and comorbidity-related gut microbiota features in college students.
INTRODUCTION: The association between body fat percentage (BFP)-defined obesity and depression in college students remains unclear, and gut microbiota alterations in this comorbid condition have not been fully characterized. METHODS: A total of 906 college students were recruited to examine the prevalence of comorbid obesity and depression and the association between body fat percentage-defined obesity and depression. Logistic regression was used for association analysis. Subsequently, 104 participants balanced for age and sex distributions across groups were selected and divided into four groups: obese with depression (G1), non-obese with depression (G2), obese without depression (G3), and non-obese without depression (G4). Fecal samples were analyzed by 16S rRNA gene sequencing. RESULTS: The prevalence of comorbid obesity and depression was 9.71%. BFP-defined obesity was significantly associated with depression after adjustment for covariates (OR = 1.62, 95% CI: 1.10-2.38). Gut microbiota analysis showed no significant differences in α-diversity among groups, whereas β-diversity differed significantly between the G1 and G4 (P < 0.05). Descriptive taxonomic profiles suggested differences in the relative abundances of several genera (e.g., decreased Akkermansia, increased Fusobacterium and Collinsella in G1). PICRUSt- based functional prediction suggested differences in inferred microbial metabolic pathways between G1 and other groups, including higher predicted lipopolysaccharide biosynthesis pathway abundance than in G2 and G4. DISCUSSION: BFP-defined obesity was associated with depression in college students. The microbiome findings were exploratory and suggest that co-occurring obesity and depression may be associated with differences in gut microbial composition and predicted functional potential. Larger longitudinal studies with direct functional and inflammatory measurements are needed.
-
Understanding How Mental Health Influences IBD Outcomes: A Review of Potential Culprit Biological Mechanisms.
Inflammatory bowel disease (IBD) includes Crohn's disease (CD) and ulcerative colitis (UC). Similar to other chronic diseases, IBD is associated with negative mental health outcomes. The prevalence of anxiety and depression with IBD is increasing in western societies and there is a growing body of evidence suggesting a bidirectional relationship which remains poorly understood. This review seeks to distil current evidence on the epidemiology, biological mechanisms and microbial changes through which anxiety and depression may lead to worse IBD outcomes. The literature demonstrates that a prior diagnosis of depression is associated with an increased risk of developing IBD. Co-morbid anxiety or depression doubles the odds of adverse outcomes in IBD. Antidepressants appear to have class dependent effects on modulating disease activity in IBD with co-morbid depression. Chronic stress may drive IBD through a number of mechanisms, including inducing the hypothalamic pituitary axis, glucocorticoid resistance, increasing intestinal permeability, and releasing inflammatory cytokines. Alterations in the microbiome on either a genus or species' level has been shown to be affected by and have an impact on both mental health illness and IBD activity. Further research with high quality longitudinal follow-up data is required to clarify causal associations of anxiety/depression and IBD onset as well as measure the impact of different antidepressant classes and microbiome targeted strategies on disease progression and outcomes.
-
Ultra-processed food exposure and adverse health outcomes: umbrella review of epidemiological meta-analyses.
OBJECTIVE: To evaluate the existing meta-analytic evidence of associations between exposure to ultra-processed foods, as defined by the Nova food classification system, and adverse health outcomes. DESIGN: Systematic umbrella review of existing meta-analyses. DATA SOURCES: MEDLINE, PsycINFO, Embase, and the Cochrane Database of Systematic Reviews, as well as manual searches of reference lists from 2009 to June 2023. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Systematic reviews and meta-analyses of cohort, case-control, and/or cross sectional study designs. To evaluate the credibility of evidence, pre-specified evidence classification criteria were applied, graded as convincing ("class I"), highly suggestive ("class II"), suggestive ("class III"), weak ("class IV"), or no evidence ("class V"). The quality of evidence was assessed using the GRADE (Grading of Recommendations, Assessment, Development, and Evaluations) framework, categorised as "high," "moderate," "low," or "very low" quality. RESULTS: The search identified 45 unique pooled analyses, including 13 dose-response associations and 32 non-dose-response associations (n=9 888 373). Overall, direct associations were found between exposure to ultra-processed foods and 32 (71%) health parameters spanning mortality, cancer, and mental, respiratory, cardiovascular, gastrointestinal, and metabolic health outcomes. Based on the pre-specified evidence classification criteria, convincing evidence (class I) supported direct associations between greater ultra-processed food exposure and higher risks of incident cardiovascular disease related mortality (risk ratio 1.50, 95% confidence interval 1.37 to 1.63; GRADE=very low) and type 2 diabetes (dose-response risk ratio 1.12, 1.11 to 1.13; moderate), as well as higher risks of prevalent anxiety outcomes (odds ratio 1.48, 1.37 to 1.59; low) and combined common mental disorder outcomes (odds ratio 1.53, 1.43 to 1.63; low). Highly suggestive (class II) evidence indicated that greater exposure to ultra-processed foods was directly associated with higher risks of incident all cause mortality (risk ratio 1.21, 1.15 to 1.27; low), heart disease related mortality (hazard ratio 1.66, 1.51 to 1.84; low), type 2 diabetes (odds ratio 1.40, 1.23 to 1.59; very low), and depressive outcomes (hazard ratio 1.22, 1.16 to 1.28; low), together with higher risks of prevalent adverse sleep related outcomes (odds ratio 1.41, 1.24 to 1.61; low), wheezing (risk ratio 1.40, 1.27 to 1.55; low), and obesity (odds ratio 1.55, 1.36 to 1.77; low). Of the remaining 34 pooled analyses, 21 were graded as suggestive or weak strength (class III-IV) and 13 were graded as no evidence (class V). Overall, using the GRADE framework, 22 pooled analyses were rated as low quality, with 19 rated as very low quality and four rated as moderate quality. CONCLUSIONS: Greater exposure to ultra-processed food was associated with a higher risk of adverse health outcomes, especially cardiometabolic, common mental disorder, and mortality outcomes. These findings provide a rationale to develop and evaluate the effectiveness of using population based and public health measures to target and reduce dietary exposure to ultra-processed foods for improved human health. They also inform and provide support for urgent mechanistic research. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42023412732.
-
Post-weaning A1/A2 β-casein milk intake modulates depressive-like behavior, brain μ-opioid receptors, and the metabolome of rats.
The postnatal period is critical for brain and behavioral development and is sensitive to environmental stimuli, such as nutrition. Prevention of weaning from maternal milk was previously shown to cause depressive-like behavior in rats. Additionally, loss of dietary casein was found to act as a developmental trigger for a population of brain opioid receptors. Here, we explore the effect of exposure to milk containing A1 and A2 β-casein beyond weaning. A1 but not A2 β-casein milk significantly increased stress-induced immobility in rats, concomitant with an increased abundance of Clostridium histolyticum bacterial group in the caecum and colon of A1 β-casein fed animals, brain region-specific alterations of μ-opioid and oxytocin receptors, and modifications in urinary biochemical profiles. Moreover, urinary gut microbial metabolites strongly correlated with altered brain metabolites. These findings suggest that consumption of milk containing A1 β-casein beyond weaning age may affect mood via a possible gut-brain axis mechanism.
-
Stress & the gut-brain axis: Regulation by the microbiome.
The importance of the gut-brain axis in regulating stress-related responses has long been appreciated. More recently, the microbiota has emerged as a key player in the control of this axis, especially during conditions of stress provoked by real or perceived homeostatic challenge. Diet is one of the most important modifying factors of the microbiota-gut-brain axis. The routes of communication between the microbiota and brain are slowly being unravelled, and include the vagus nerve, gut hormone signaling, the immune system, tryptophan metabolism, and microbial metabolites such as short chain fatty acids. The importance of the early life gut microbiota in shaping later health outcomes also is emerging. Results from preclinical studies indicate that alterations of the early microbial composition by way of antibiotic exposure, lack of breastfeeding, birth by Caesarean section, infection, stress exposure, and other environmental influences - coupled with the influence of host genetics - can result in long-term modulation of stress-related physiology and behaviour. The gut microbiota has been implicated in a variety of stress-related conditions including anxiety, depression and irritable bowel syndrome, although this is largely based on animal studies or correlative analysis in patient populations. Additional research in humans is sorely needed to reveal the relative impact and causal contribution of the microbiome to stress-related disorders. In this regard, the concept of psychobiotics is being developed and refined to encompass methods of targeting the microbiota in order to positively impact mental health outcomes. At the 2016 Neurobiology of Stress Workshop in Newport Beach, CA, a group of experts presented the symposium "The Microbiome: Development, Stress, and Disease". This report summarizes and builds upon some of the key concepts in that symposium within the context of how microbiota might influence the neurobiology of stress.
-
Disentangling What We Know About Microbes and Mental Health.
Much has been written in recent years about the gut-brain axis. Exciting pilot studies suggest probiotic applications to the gut can reduce anxiety and depression via the vagus nerve. But not to diminish such findings, much still needs to be considered, including the fact that the vagus nerve links to many other body sites that also host a microbiome. Questions remain that touch the core of being human: (i) Do our microbes influence happiness and to what extent? (ii) What components of the gut microbiota and their function, including as it relates to mental health, are critical and how do they differ between agile, fit hunter gatherers and obese westerners or Danes described as the happiest people on the planet? (iii) What role do environmental pollutants play in this microbes-host ecosystem? While approaching life from a reductionist perspective has a long history in science, we need to try to interrogate these health and disease issues from a wider perspective. For verification of a link between the gut microbiota and brain, and to test new therapies, human studies are needed, and are long overdue.
-
Neuromicrobiology: How Microbes Influence the Brain.
We review here recent discoveries in the exciting new field of neuromicrobiology. This field encompasses the interactions between the microbiome and the central nervous system. The microbiome has a tremendous impact on human health. In particular, the gut microbiota may play a key role in many essential processes in health and disease via the activity of the gut-brain axis, possibly contributing to autism spectrum disorders, Alzheimer's disease, Parkinson's disease, depression, and anxiety disorder. Gut microbes may also be involved in nociception, complex host behaviors, and brain development. Future efforts will be needed to determine whether the observed associations correspond to causative mechanisms, as well as to engineer effective interventions to modulate the effects of the microbiome on the central nervous system.
-
The Role of Gut Microbiota in the High-Risk Construct of Severe Mental Disorders: A Mini Review.
Severe mental disorders (SMD) are highly prevalent psychiatric conditions exerting an enormous toll on society. Therefore, prevention of SMD has received enormous attention in the last two decades. Preventative approaches are based on the knowledge and detailed characterization of the developmental stages of SMD and on risk prediction. One relevant biological component, so far neglected in high risk research, is microbiota. The human microbiota consists in the ensemble of microbes, including viruses, bacteria, and eukaryotes, that inhabit several ecological niches of the organism. Due to its demonstrated role in modulating illness and health, as well in influencing behavior, much interest has focused on the characterization of the microbiota inhabiting the gut. Several studies in animal models have shown the early modifications in the gut microbiota might impact on neurodevelopment and the onset of deficits in social behavior corresponding to distinct neurosignaling alterations. However, despite this evidence, only one study investigated the effect of altered microbiome and risk of developing mental disorders in humans, showing that individuals at risk for SMD had significantly different global microbiome composition than healthy controls. We then offer a developmental perspective and provided mechanistic insights on how changes in the microbiota could influence the risk of SMD. We suggest that the analysis of microbiota should be included in the comprehensive assessment generally performed in populations at high risk for SMD as it can inform predictive models and ultimately preventative strategies.