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Fermented Vegetables as a Source of Psychobiotics: A Review of the Evidence for Mental Health Benefits.
The human gut microbiome, comprised of trillions of microorganisms, plays a pivotal role in both physical and mental health. Recent research underscores the intriguing connection between gut bacteria and mental well-being, leading to the emergence of psychobiotics-microbes with mental health benefits. This review aims to explore fermented vegetables, a traditional dietary staple experiencing renewed interest, as a potential source of psychobiotics. Fermentation alters the microbial composition of vegetables, enriching them with beneficial bacteria such as Lactobacillus and Bifidobacterium. Various fermented vegetables, including kimchi, sauerkraut, and tempeh, host distinct bacterial communities. The review investigates how these psychobiotics may impact mental health through the gut-brain axis, a communication network between the gut and the central nervous system. Possible mechanisms encompass neurotransmitter modulation (e.g., serotonin, GABA), inflammation reduction and immunity modulation, and stress response enhancement through the hypothalamic-pituitary adrenal (HPA) axis. Clinical studies exploring the influence of fermented vegetables on mental health outcomes, including anxiety, depression, and cognitive function, are critically evaluated. The review assesses the efficacy of different fermented vegetables and probiotic strains while recognizing limitations in existing research and the necessity for further investigation.
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Probiotics: Potential novel therapeutics for microbiota-gut-brain axis dysfunction across gender and lifespan.
Probiotics are live microorganisms, which when administered in adequate amounts, present a health benefit for the host. While the beneficial effects of probiotics on gastrointestinal function are generally well recognized, new animal research and clinical studies have found that alterations in gut microbial communities can have a broad range of effects throughout the body. Non-intestinal sites impacted include the immune, endocrine, cardiovascular and the central nervous system (CNS). In particular, there has been a growing interest and appreciation about the role that gut microbiota may play in affecting CNS-related function through the 'microbiota-gut-brain axis'. Emerging evidence suggests potential therapeutic benefits of probiotics in several CNS conditions, such as anxiety, depression, autism spectrum disorders and Parkinson's disease. There may also be some gender-specific variances in terms of probiotic mediated effects, with the gut microbiota shaping and being concurrently molded by the hormonal environment governing differences between the sexes. Probiotics may influence the ability of the gut microbiome to affect a variety of biological processes in the host, including neurotransmitter activity, vagal neurotransmission, generation of neuroactive metabolites and inflammatory response mediators. Some of these may engage in cross talk with host sex hormones, such as estrogens, which could be of relevance in relation to their effects on stress response and cognitive health. This raises the possibility of gender-specific variation with regards to the biological action of probiotics, including that on the endocrine and central nervous systems. In this review we aim to describe the current understanding in relation to the role and use of probiotics in microbiota-gut-brain axis-related dysfunction. Furthermore, we will address the conceptualization and classification of probiotics in the context of gender and lifespan as well as how restoring gut microbiota composition by clinical or dietary intervention can help in supporting health outcomes other than those related to the gastrointestinal tract. We also evaluate how these new learnings may impact industrial effort in probiotic research and the discovery and development of novel and more personalized, condition-specific, beneficial probiotic therapeutic agents.
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The Postpartum Maternal and Newborn Microbiomes.
Biological and environmental changes to maternal and newborn microbiomes in the postnatal period can affect health outcomes for the mother-baby dyad. Postpartum sleep deprivation and unmet dietary needs can alter commensal bacteria within the body and disrupt gut-brain communication. Perineal injury and breast infections also change microbial community composition, potentiating an environment favoring pathogen growth. The gut microbiome refers to the collection of microorganisms working in harmony. Disruptions within the gut microbiome and gut-brain communication may lead to postpartum depression, a potentially devastating sequela. Postnatal newborn changes to the gut and skin microbiome materialize quickly after birth and are profoundly influenced by mode of birth, feeding method, and bathing and skin care practices. During the newborn period, infant microbiomes are highly vulnerable and susceptible to multiple influences. Maternal-newborn nurses have a valuable role in helping mothers and newborns promote healthy microbiomes. Factors that influence the rapidly changing postnatal microbiome of the mother and her newborn, and the role nurses have to positively influence immediate and long-term health outcomes are presented.
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The effects of psychobiotics on the microbiota-gut-brain axis in early-life stress and neuropsychiatric disorders.
Psychobiotics are considered among potential avenues for modulating the bidirectional communication between the gastrointestinal tract and central nervous system, defined as the microbiota-gut-brain axis (MGBA). Even though causality has not yet been established, intestinal dysbiosis has emerged as a hallmark of several diseases, including neuropsychiatric disorders (NPDs). The fact that the microbiota and central nervous system are co-developing during the first years of life has provided a paradigm suggesting a potential role of psychobiotics for earlier interventions. Studies in animal models of early-life stress (ELS) have shown that they can counteract the pervasive effects of stress during this crucial developmental period, and rescue behavioral symptoms related to anxiety and depression later in life. In humans, evidence from clinical studies on the efficacy of psychobiotics at improving mental outcomes in most NPDs remain limited, except for major depressive disorder for which more studies are available. Consequently, the beneficial effect of psychobiotics on depression-related outcomes in adults are becoming clearer. While the specific mechanisms at play remain elusive, the effect of psychobiotics are generally considered to involve the hypothalamic-pituitary-adrenal axis, intestinal permeability, and inflammation. It is anticipated that future clinical studies will explore the potential role of psychobiotics at mitigating the risk developing NPDs in vulnerable individuals or in the context of childhood adversity. However, such studies remain challenging at present in terms of design and target populations; the profound impact of stress on the proper development of the MGBA during the first year of life is becoming increasingly recognized, but the trajectories post-ELS in humans and the mechanisms by which stress affects the susceptibility to various NPDs are still ill-defined. As psychobiotics are likely to exert both shared and specific mechanisms, a better definition of target subpopulations would allow to tailor psychobiotics selection by aligning mechanistic properties with known pathophysiological mechanisms or risk factors. Here we review the available evidence from clinical and preclinical studies supporting a role for psychobiotics at ameliorating depression-related outcomes, highlighting the knowledge gaps and challenges associated with conducting longitudinal studies to address outstanding key questions in the field.
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Nonylphenol induces depressive behavior in rats and affects gut microbiota: A dose-dependent effect.
Nonylphenol (NP), an endocrine disruptor absorbed through food intake, was investigated in this study for its potential dose-response relationship with the manifestation of depression-like behavior in rats. Based on this, the mechanisms of NP-induced depressive behavior, encompassing neurotransmitters, gut barrier function, inflammatory response, gut microbiota composition and metabolites were further explored. At medium and high NP doses, both mRNA and protein levels of zonula occludens protein-1 and claudin-1 were considerably downregulated, concomitant with an elevation in tumor necrosis factor-α and interleukin-1β expression in a dose-dependent effect, resulting in damage to the gut mucosa. Despite a minimal impact on behavior and gut barriers at low NP doses, alterations in gut microbiota composition were observed. During NP exposure, dose-dependent changes in the gut microbiota revealed a decline in microbial diversity linked to the synthesis of short-chain fatty acids. NP not only adversely affected the gut microbiota structure but also exacerbated central nervous system damage through the gut-brain axis. The accumulation of NP may cause neurotransmitter disturbances and inflammatory responses in the hippocampus, which also exacerbate depressed behavior in rats. Therefore, NP could exacerbate the inflammatory response in the hippocampus and colon by compromising intestinal barrier integrity, facilitating the proliferation of pathogenic bacteria, impairing butyrate metabolism, and perturbing neurotransmitter homeostasis, thus aggravating the depressive behavior of rats. It is noteworthy that the changes in these indicators were related to the NP exposure dose.
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Manipulations of the gut microbiome alter chemotherapy-induced inflammation and behavioral side effects in female mice.
Chemotherapy treatment is associated with acute behavioral side effects (fatigue, anorexia) that significantly reduce patient quality of life and are dose-limiting, thereby increasing mortality (Kidwell et al., 2014). Disruptions to gut homeostasis (diarrhea, constipation, microbial dysbiosis) are also observed in patients receiving chemotherapy. In non-oncological patients, facets of mental health (fatigue, anxiety, depression) correlate with alterations in the gut microbiome, suggestive of a contribution of the gut in CNS disease etiology. The potential gut-to-brain pathway is poorly understood in patients receiving chemotherapy. Our prior studies have demonstrated a correlation between chemotherapy treatment, gut changes, peripheral and central inflammation, and behavioral symptoms in mice. Here we aimed to determine the extent to which chemotherapy-associated gut manipulations modulate the behavioral and biological consequences of chemotherapy. We measured sickness behaviors, peripheral and central inflammatory mediators, and anxiety in conventional or germ-free female mice: 1) cohabitating with mice of the opposite treatment group, 2) pre-treated with broad-spectrum antibiotics, or 3) given an intra-gastric gavage of gut content from chemotherapy-treated mice. In cohabitation studies, presumed coprophagia promoted body mass recovery, however strong associations with inflammation and behavior were not observed. Reduction of gut microbial alpha diversity via antibiotics did not prevent chemotherapy-associated side effects, however the relative abundances of the genera Tyzzerella, Romboutsia, and Turicibacter correlated with circulating inflammatory (IL-1β) and behavioral outcomes (lethargy, anxiety-like behavior). A gut microbiota transplant from chemotherapy-treated mice decreased central locomotion in open field testing, increased circulating CXCL1, and increased hippocampal Il6 and Tnfa in germ-free mice compared to germ-free mice that received a transplant from vehicle-treated mice. Taken together, these data provide further evidence that the gut microbiota likely contributes to the development of chemotherapy-associated side effects. This work has significant implications in the future treatment of anxiety in patients, and warrants future studies using microbe-based treatment options.
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GABA-Producing Bacteria as Potential Psychobiotics in Gut-Brain Axis Regulation.
γ-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the central nervous system (CNS) and plays a vital role in maintaining neural balance, regulating mood, and reducing stress responses. Recent metagenomic studies of the gut microbiome have shown that various bacterial species, especially those in the genera Lactobacillus, Bifidobacterium, and Bacteroides, isolated from the human gut and environmental sources such as fermented foods, contain glutamate decarboxylase (GAD) systems that enable GABA production. Microbially produced GABA can influence the microbiota-gut-brain (MGB) axis by activating neural, endocrine, and immune signalling pathways that are crucial for maintaining gut and brain homeostasis. Emerging evidence suggests that supplementation with GABA-producing bacteria, known as psychobiotics, may improve neurotransmitter balance, modulate cytokine production, strengthen the integrity of the intestinal barrier, and alleviate anxiety- and depression-related behaviours. This review summarises current knowledge of GABA-producing bacterial strains derived from the human gut and food environments and explores their potential as emerging psychobiotics in modulating gut-brain communication and mental health.
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Decreased Gut Microbiome Tryptophan Metabolism and Serotonergic Signaling in Patients With Persistent Mental Health and Gastrointestinal Symptoms After COVID-19.
INTRODUCTION: An estimated 15%-29% of patients report new gastrointestinal (GI) symptoms after coronavirus-19 disease (COVID-19) while 4%-31% report new depressive symptoms. These symptoms may be secondary to gut microbiome tryptophan metabolism and 5-hydroxytryptamine (5-HT)-based signaling. METHODS: This study used specimens from 2 patient cohorts: (i) fecal samples from patients with acute COVID-19 who participated in a randomized controlled trial testing prebiotic fiber and (ii) blood samples from patients with acute COVID-19. Six months after recovering from COVID-19, both cohorts answered questions related to GI symptoms and anxiety or depression. Microbiome composition and function, focusing on tryptophan metabolism-associated pathways, and plasma 5-HT were assessed. RESULTS: In the first cohort (n = 13), gut microbiome L-tryptophan biosynthesis during acute COVID-19 was decreased among those who developed more severe GI symptoms (2.0-fold lower log activity comparing those with the most severe GI symptoms vs those with no symptoms, P = 0.06). All tryptophan pathways showed decreased activity among those with more GI symptoms. The same pathways were also decreased in those with the most severe mental health symptoms after COVID-19. In an untargeted analysis, 5 additional metabolic pathways significantly differed based on subsequent development of GI symptoms. In the second cohort (n = 39), plasma 5-HT concentration at the time of COVID-19 was increased 5.1-fold in those with GI symptoms alone compared with those with mental health symptoms alone ( P = 0.02). DISCUSSION: Acute gut microbiome-mediated reduction in 5-HT signaling may contribute to long-term GI and mental health symptoms after COVID-19. Future studies should explore modification of 5-HT signaling to reduce post-COVID symptoms.
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Fructooligosaccharide ameliorates estrogen-gut-microbiome-brain axis dysfunction in estrogen-deficient rats.
Reduced levels of circulating gonadal hormones in post-menopausal women can negatively affect various physiological functions, including brain and gut deficits. There is an urgent need to find novel strategies to mitigate estrogen-gut-microbiome-brain axis (EGMBA) dysfunction. This study aimed to investigate the effect of fructooligosaccharide (FOS), a non-digestible prebiotic fiber, on estrogen deficiency-induced alterations in the EGMBA using an ovariectomized (OVX) rat model. Adult female SD rats were bilaterally OVX to induce estrogen deficiency and associated EGMBA dysfunction. Rats were administered FOS (50 mg kg-1 p.o.-1) for 28 consecutive days. To assess EGMBA dysfunction, after 28 days, we performed behavioral tests, biochemical estimations (oxidative stress), molecular estimations (inflammatory markers via ELISA), gene expression analysis (HPA axis, monoamine neurotransmission, apoptosis, gut microbiota alterations, & gut barrier integrity via RT-PCR/qPCR), and histopathological analysis. Administration of FOS significantly improved behavioral outcomes (reducing anxiety and depression, and improving memory). FOS also attenuates oxidative stress and inflammatory markers. FOS regulates apoptosis (upregulation of BCL-2 and downregulation of Bax), HPA axis functioning (corticosterone, GR, MR, & CRH), and monoamine neurotransmission (MAO-A & COMT) in the hippocampus of OVX rats. FOS also promoted healthy cell growth and prevented apoptosis. Additionally, FOS restored gut microbial eubiosis, improved mucus secretion (MUC-2), preserved tight junction protein expression (Lipocalin-2, Claudin, & TLR-4), and maintained the colon microstructure. FOS exerts multifaceted protective effects on the EGMBA by modulating gut and brain functions. These findings support its potential as a non-hormonal therapeutic approach for managing postmenopausal complications.
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Vancomycin-Induced Changes in Host Immunity and Behavior: Comparative Genomic and Metagenomic Analysis in C57BL/6 and BALB/c Mice.
BACKGROUND: The consequence of treatment with antibiotics on the gut microbiota can be destructive. The antibiotics, however, can be utilized to understand the role of gut microbiota on the host physiology. AIM: Earlier, we reported the efficacy of vancomycin in gut microbiota perturbation. We continued to understand the effect of restoration kinetics of perturbed gut microbiota on the immunity and behavior of Th1 (C57BL/6)- and Th2 (BALB/c)-biased mice. METHODS: We studied restoration kinetics of the gut microbiota for two months following the withdrawal of vancomycin treatment in both mice strains. We analyzed cecal microbiome composition, different behavioral assays, and expression of select genes associated with stress and barrier function in gut and brain. RESULTS: Metagenomic analysis of gut microbiota revealed that the treatment with vancomycin caused a significant decrease in the relative abundance of Firmicutes and Bacteroidetes phyla with a time-dependent increase in Proteobacteria and Verrucomicrobia phyla. Maximum restoration (> 70%) of gut microbiota happened by the 15th day of withdrawal of vancomycin. BALB/c mice showed a more efficient restoration of gut microbiota compared to C57BL/6 mice. We established the correlation patterns of gut microbiota alteration and its effect on (a) the behavior of mice, (b) expression of key brain molecules, and (c) immunity-related genes. CONCLUSIONS: The results revealed that the gut microbiome profiling, behavior, and immune responses varied significantly between Th1- and Th2-biased mice. By withdrawing the treatment with vancomycin of major gut microbes, important physiological and behavioral changes of both mice strains returned to the normal (untreated control) level.