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Gut Feelings: How Microbiota Might Impact the Development and Course of Anorexia Nervosa.
Anorexia nervosa (AN) can probably be regarded as a "model" for studying the interaction of nutrition with the gut-brain axis, which has drawn increased attention from researchers and clinicians alike. The gut microbiota influences somatic effects, such as energy extraction from food and body weight gain, as well as appetite, gut permeability, inflammation and complex psychological behaviors, such as depression or anxiety, all of which play important roles in AN. As nutrition is one of the main factors that influence the gut microbiota, nutritional restriction and selective eating in AN are likely influencing factors; however, nutritional rehabilitation therapy is surprisingly understudied. Here, we review the general mechanisms of the interactions between nutrition, the gut microbiota and the host that may be relevant to AN, paying special attention to the gut-brain axis, and we present the first specific findings in patients with AN and corresponding animal models. In particular, nutritional interventions, including food selection, supplements, and pre-, pro- and synbiotics that have the potential to influence the gut microbiota, are important research targets to potentially support future AN therapy.
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Modifiable Risk Factors for Dementia: The Role of Gut Microbiota.
Dementia is a syndrome resulting from chronic or progressive brain disease. Around 40% of worldwide dementia can be prevented or delayed by modifying 12 risk factors: low educational attainment in early life, mid-life hypertension, mid-life obesity, hearing loss, traumatic brain injury, excessive alcohol consumption, smoking, depression, physical inactivity, social isolation, diabetes mellitus, and air pollution. There is growing evidence that gastrointestinal tract microbiota may significantly contribute to dementia pathogenesis. In particular, gut dysbiosis can trigger metabolic diseases and the progression of low-grade systemic inflammation, being involved in much of the major modifiable risk factors. In this review, we focus on studies that have evaluated the association between modifiable risk factors for dementia and the role of gut microbiota. We also suggest clinical implications for researchers in dementia-gut microbiota related fields.
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Examining the Influence of the Human Gut Microbiota on Cognition and Stress: A Systematic Review of the Literature.
The gut microbiota is seen as an emerging biotechnology that can be manipulated to enhance or preserve cognition and physiological outputs of anxiety and depression in clinical conditions. However, the existence of such interactions in healthy young individuals in both non-stressful and stressful environments is unclear. The aim of this systematic review was to examine the relationship between the human gut microbiota, including modulators of the microbiota on cognition, brain function and/or stress, anxiety and depression. A total of n = 25 eligible research articles from a possible 3853 published between October 2018 and August 2021 were identified and included. Two study design methods for synthesis were identified: cross-sectional or pre/post intervention. Few cross-sectional design studies that linked microbiota to cognition, brain activity/structure or mental wellbeing endpoints existed (n = 6); however, correlations between microbiota diversity and composition and areas of the brain related to cognitive functions (memory and visual processing) were observed. Intervention studies targeting the gut microbiota to improve cognition, brain structure/function or emotional well-being (n = 19) generally resulted in improved brain activity and/or cognition (6/8), and improvements in depression and anxiety scores (5/8). Despite inherit limitations in studies reviewed, available evidence suggests that gut microbiota is linked to brain connectivity and cognitive performance and that modulation of gut microbiota could be a promising strategy for enhancing cognition and emotional well-being in stressed and non-stressed situations.
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Gut microbiota alteration and modulation in psychiatric disorders: Current evidence on fecal microbiota transplantation.
The micro-organisms residing within the gastrointestinal tract, namely gut microbiota, form a dynamic population proper of each individual, mostly composed by bacteria which co-evolved symbiotically with human species. The advances of culture-independent techniques allowed the understanding of the multiple functions of the gut microbiota in human physiology and disease, the latter often recognising a predisposing condition in an imbalanced intestinal microbial ecosystem (dysbiosis). A complex mutual interconnection between the central nervous system (CNS), the intestine and the gut microbiota, known as "microbiota-gut-brain axis", has been hypothesized to play a pivotal role in maintaining central and peripheral functions, as well as mental health. Thus, dysbiosis with specific microbiota imbalances seems to be strongly associated with the onset psychiatric disorders by altering neurodevelopment, enhancing neurodegeneration, affecting behaviour and mood. Fecal microbiota transplantation (FMT) consists of transferring the fecal matter from a donor into the gastrointestinal tract of a recipient, and it is used to quickly modulate the gut microbiota. This review focuses on the uses of FMT in psychiatric disorders. FMT has been used to induce dysbiosis and to study the disease development, or to heal dysbiosis-related mental disorders. Overall, FMT of impaired microbiota resulted effective in enhancing psychiatric-like disturbances (mainly depression and anxiety) in recipient animals, plausibly by impairing immune system, inflammatory and metabolic pathways, neurochemical processes and neuro-transmission. On the other side, preclinical and clinical data suggest that reversing or mitigating dysbiosis seems a promising strategy to restore behavioural impairments or to obtain psychiatric symptom relief. However, current evidence is limited by the lack of procedural standardization, the paucity of human studies in the vastity of psychiatric conditions and the need of a microbiota-targeted donor-recipient matching.
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Obesity and mental health improvement following nutritional education focusing on gut microbiota composition in Japanese women: a randomised controlled trial.
PURPOSE: Gut microbiota composition was supposedly related to obesity and psychological factors. We examined the effects of a nutritional education intervention focusing on gut microbiota composition on obesity and psychological factors among obese women. METHODS: Forty-four obese Japanese women aged 40 or older were randomly assigned to either an intervention group (n = 22) or control group (n = 22). The intervention consisted of a 20-min dietary lecture and a 10-min counselling session by registered dieticians, every 2 weeks for eight consecutive weeks. Body weight, height, waist circumference, food frequency, and gut microbiota composition were measured, and self-rated health and psychological factors were scored before and after the intervention. RESULTS: All participants completed the 8 week program. After the intervention, dietary fibre intake (p < 0.01), frequency of vegetable consumption (p = 0.020), and frequency of milk and milk product consumption (p < 0.01) increased significantly in the intervention group compared with the control group. Body weight and body mass index (BMI; p < 0.001), waist circumference (p < 0.01), and the depression scale score (p < 0.01) decreased significantly, while significant improvements were found in self-rated health (p = 0.045) and microbiome diversity (p < 0.01). CONCLUSION: Nutritional education focusing on gut microbiota composition may improve obesity and psychological factors in obese women.
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Probiotics, Live Biotherapeutic Products (LBPs), and Gut-Brain Axis Related Psychological Conditions: Implications for Research and Dietetics.
It is well-known that probiotics have key roles in the crosstalk between the gut and brain in terms of nutrition and health. However, when investigating their role in nutrition and health, it can be important to discriminate probiotics used as foods, food supplements, or drugs. For clarification of this terminology, the Food and Drug Administration (FDA) has established a new "live biotherapeutic products" (LBP) category, expressing pharmaceutical expectations and to reduce confusion in the literature. Growing evidence advises that the community of microorganisms found in the gut microbiota is associated with psychological conditions. Hence, it is thought that LBPs may positively affect depression, anxiety, bipolar disorder, and schizophrenia by reducing inflammation, improving gut microbiota, and balancing gut neurometabolites. This review focuses on the specific position of probiotics as LBPs in psychological conditions. Condition-specific potential pathways and mechanisms of LBPs and the prominent strains are discussed in the light of novel studies for future research, dietetic and pharmaceutical applications.
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Bridging the Mind and Gut: Uncovering the Intricacies of Neurotransmitters, Neuropeptides, and their Influence on Neuropsychiatric Disorders.
BACKGROUND: The gut-brain axis (GBA) is a bidirectional signaling channel that facilitates communication between the gastrointestinal tract and the brain. Recent research on the gut-brain axis demonstrates that this connection enables the brain to influence gut function, which in turn influences the brain and its cognitive functioning. It is well established that malfunctioning of this axis adversely affects both systems' ability to operate effectively. OBJECTIVE: Dysfunctions in the GBA have been associated with disorders of gut motility and permeability, intestinal inflammation, indigestion, constipation, diarrhea, IBS, and IBD, as well as neuropsychiatric and neurodegenerative disorders like depression, anxiety, schizophrenia, autism, Alzheimer's, and Parkinson's disease. Multiple research initiatives have shown that the gut microbiota, in particular, plays a crucial role in the GBA by participating in the regulation of a number of key neurochemicals that are known to have significant effects on the mental and physical well-being of an individual. METHODS: Several studies have investigated the relationship between neuropsychiatric disorders and imbalances or disturbances in the metabolism of neurochemicals, often leading to concomitant gastrointestinal issues and modifications in gut flora composition. The interaction between neurological diseases and gut microbiota has been a focal point within this research. The novel therapeutic interventions in neuropsychiatric conditions involving interventions such as probiotics, prebiotics, and dietary modifications are outlined in this review. RESULTS: The findings of multiple studies carried out on mice show that modulating and monitoring gut microbiota can help treat symptoms of such diseases, which raises the possibility of the use of probiotics, prebiotics, and even dietary changes as part of a new treatment strategy for neuropsychiatric disorders and their symptoms. CONCLUSION: The bidirectional communication between the gut and the brain through the gut-brain axis has revealed profound implications for both gastrointestinal and neurological health. Malfunctions in this axis have been connected to a range of disorders affecting gut function as well as cognitive and neuropsychiatric well-being. The emerging understanding of the role of gut microbiota in regulating key neurochemicals opens up possibilities for novel treatment approaches for conditions like depression, anxiety, and neurodegenerative diseases.
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Gut microbiota modulates neurotransmitter and gut-brain signaling.
Neurotransmitters, including 5-hydroxytryptamine (5-HT), dopamine (DA), gamma-aminobutyric acid (GABA), and glutamate, are essential transductors in the Gut-Brain Axis (GBA), playing critical roles both peripherally and centrally. Accumulating evidence suggests that the gut microbiota modulates intestinal neurotransmitter metabolism and gut-to-brain signaling, shedding light on the crucial role of the gut microbiota in brain function and the pathogenesis of various neuropsychiatric diseases, such as major depression disorder (MDD), anxiety, addiction and Parkinson's disease (PD). Despite the exciting findings, the mechanisms underlying the modulation of neurotransmitter metabolism and function by the gut microbiota are still being elucidated. In this review, we aim to provide a comprehensive overview of the existing knowledge about the role of the gut microbiota in neurotransmitter metabolism and function in animal and clinical experiments. Moreover, we will discuss the potential mechanisms through which gut microbiota-derived neurotransmitters contribute to the pathogenesis of neuropsychiatric diseases, thus highlighting a novel therapeutic target for these conditions.
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Effects of heat stress and depressed feed intake on the cecal and ileal microbiota of broiler chickens.
Chronic heat stress (HS) is known to depress feed intake (FI) and growth in broiler chickens, and may alter the gut microbiota and health, however, the amplitude and duration of each (HS and depressed FI) effect on gut microbiota is still unclear. This study aimed to determine the effects of chronic and acute HS on the cecal and ileal microbiota profiles. Broilers were subjected to thermoneutral (TN, 23°C) or chronic cyclic HS (CHS, 8 h/d, 35°C) condition from d29-42, and one group to acute HS (AHS, 2 h, 35°C) at d42. To distinguish between the effect of HS and FI, one pair-fed (PF) group (maintained at TN condition but had similar FI as CHS birds) was used from d29-42. Chronic HS decreased richness in the cecal microbiota compared to TN, while PF did not, and AHS led to higher richness compared to CHS. Acute HS and PF altered cecal microbiota profiles similarly to CHS under weighted UniFrac. In the ileum, PF altered microbiota under unweighted UniFrac, and CHS further altered microbiota. Decreased Lactobacillus and increased Ligilactobacillus were observed with CHS, AHS, and PF in the cecum. Chronic HS may influence different predicted metabolic pathways compared to PF, while AHS shared some similarities with CHS. Understanding both the direct effects of CHS and indirect effects through depressed FI, along with the short-term effects from AHS, will be of importance in devising nutritional strategies to maintain gut microbial balance and limit negative effects to broiler chickens' performance and health.
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The metabolome-wide signature of major depressive disorder.
Major Depressive Disorder (MDD) is a common, frequently chronic condition characterized by substantial molecular alterations and pathway dysregulations. Single metabolite and targeted metabolomics platforms have revealed several metabolic alterations in depression, including energy metabolism, neurotransmission, and lipid metabolism. More comprehensive coverage of the metabolome is needed to further specify metabolic dysregulations in depression and reveal previously untargeted mechanisms. Here, we measured 820 metabolites using the metabolome-wide Metabolon platform in 2770 subjects from a large Dutch clinical cohort with extensive clinical phenotyping (1101 current MDD, 868 remitted MDD, 801 healthy controls) at baseline, which were repeated in 1805 subjects at 6-year follow up (327 current MDD, 1045 remitted MDD, 433 healthy controls). MDD diagnosis was based on DSM-IV psychiatric interviews. Depression severity was measured with the Inventory of Depressive Symptomatology Self-report. Associations between metabolites and MDD status and depression severity were assessed at baseline and at 6-year follow-up. At baseline, 139 and 126 metabolites were associated with current MDD status and depression severity, respectively, with 79 overlapping metabolites. Adding body mass index and lipid-lowering medication to the models changed results only marginally. Among the overlapping metabolites, 34 were confirmed in internal replication analyses using 6-year follow-up data. Downregulated metabolites were enriched with long-chain monounsaturated (P = 6.7e-07) and saturated (P = 3.2e-05) fatty acids; upregulated metabolites were enriched with lysophospholipids (P = 3.4e-4). Mendelian randomization analyses using genetic instruments for metabolites (N = 14,000) and MDD (N = 800,000) showed that genetically predicted higher levels of the lysophospholipid 1-linoleoyl-GPE (18:2) were associated with greater risk of depression. The identified metabolome-wide profile of depression indicated altered lipid metabolism with downregulation of long-chain fatty acids and upregulation of lysophospholipids, for which causal involvement was suggested using genetic tools. This metabolomics signature offers a window on depression pathophysiology and a potential access point for the development of novel therapeutic approaches.