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A Comprehensive Review of Fortification, Bioavailability, and Health Benefits of Folate.
Folate is an essential vitamin involved in one-carbon metabolism. It can be acquired from many food sources or in synthetic form. A wide range of processing methods have been studied to improve the bioaccessibility and bioavailability of folate in foods, yet this is often accompanied by a decrease in stability. Encapsulation technology has emerged as an effective solution for protecting folate from degradation and liberation while also improving its bioavailability. Folate deficiency is a prevalent phenomenon worldwide, particularly in underprivileged countries, leading to various health problems, such as neural tube defects. Thus, folate was fortified through both exogenous addition and biofortification. Gene editing technology, especially CRISPR-Cas9, has great promise in this field when compared to transgenic engineering, because transgenic engineering may pose safety concerns and environmental risks. While ongoing research has identified additional potential effects of folate, the dosage and duration remain important factors to consider for optimal health outcomes. The mechanisms of how folate promotes the production of neurotransmitters associated with the gut microbiota-brain axis and reduces depression are not well understood. In addition to folate alone, there may be synergistic effects of combined supplementation of folate and other nutrients or medications, but this is not yet fully clarified and requires further examination. This review summarizes the food sources, enrichment, bioaccessibility, and bioavailability of folate. Furthermore, the health benefits of folate, including neural tube protection, cardiovascular protection, neuroprotection, anti-cancer, immune response augmentation, and gut homeostasis maintenance, with their potential bioactivity mechanisms, are discussed.
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Microglia and gut microbiota: A double-edged sword in Alzheimer's disease.
The strong association between gut microbiota (GM) and brain functions such as mood, behaviour, and cognition has been well documented. Gut-brain axis is a unique bidirectional communication system between the gut and brain, in which gut microbes play essential role in maintaining various molecular and cellular processes. GM interacts with the brain through various pathways and processes including, metabolites, vagus nerve, HPA axis, endocrine system, and immune system to maintain brain homeostasis. GM dysbiosis, or an imbalance in GM, is associated with several neurological disorders, including anxiety, depression, and Alzheimer's disease (AD). Conversely, AD is sustained by microglia-mediated neuroinflammation and neurodegeneration. Further, GM and their products also affect microglia-mediated neuroinflammation and neurodegeneration. Despite the evidence connecting GM dysbiosis and AD progression, the involvement of GM in modulating microglia-mediated neuroinflammation in AD remains elusive. Importantly, deciphering the mechanism/s by which GM regulates microglia-dependent neuroinflammation may be helpful in devising potential therapeutic strategies to mitigate AD. Herein, we review the current evidence regarding the involvement of GM dysbiosis in microglia activation and neuroinflammation in AD. We also discuss the possible mechanisms through which GM influences the functioning of microglia and its implications for therapeutic intervention. Further, we explore the potential of microbiota-targeted interventions, such as prebiotics, probiotics, faecal microbiota transplantation, etc., as a novel therapeutic strategy to mitigate neuroinflammation and AD progression. By understanding and exploring the gut-brain axis, we aspire to revolutionize the treatment of neurodegenerative disorders, many of which share a common theme of microglia-mediated neuroinflammation and neurodegeneration.
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Oral administration of Lactococcus lactis WHH2078 alleviates depressive and anxiety symptoms in mice with induced chronic stress.
Depression is a mood disorder with a high prevalence rate globally, which is associated with abnormalities in 5-hydroxytryptamine (5-HT) metabolism. Emerging evidence suggests that certain probiotics that modulate 5-HT metabolism confer beneficial effects on depression. In this study, in vitro enterochromaffin RIN14B cells were used for screening potential antidepressant probiotic Lactococcus lactis strains. The L. lactis strain WHH2078 increased to high levels the 5-HT precursor 5-hydroxytryptophan (5-HTP) and the expression of tryptophan hydroxylase 1 (Tph1), which converts tryptophan to 5-HTP in RIN14B cells. The oral administration of WHH2078 (1 × 109 CFU mL-1) in mice with induced chronic unpredictable mild stress (CUMS) for 5 weeks significantly ameliorated depressive and anxiety-like behaviors in the tail suspension test, forced swim test, sucrose preference test, and open field test. Besides, WHH2078 significantly reduced the serum corticosterone level and restored the central levels of 5-HT, 5-HTP, and brain-derived neurotrophic factor in CUMS-induced mice. Moreover, WHH2078 also reversed the 5-HTP levels in the serum and colon, accompanied by an upregulation in colonic Tph1 gene expression. Using 16S rRNA high-throughput sequencing of feces, WHH2078 was shown to improve the CUMS-induced gut microbial dysbiosis, through restoring alpha diversity and the abundances of Firmicutes and Bacteroidetes. In summary, these results indicate that WHH2078 can alleviate rodent depressive and anxiety-like behaviors in response to CUMS, which is associated with the improvement of 5-HT metabolism and modulation of the gut microbiome composition. Therefore, supplementation of the L. lactis strain WHH2078 with antidepressant properties may serve as a promising therapeutic strategy for chronic stress-induced depression.
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Microbiota-brain interaction: The role of gut-derived proteins in addressing various neurological disorders including Parkinson's (PD) and Alzheimer's diseases (AD).
The microbiota-brain interaction is a complex network connecting gut microbiota to the enteric nervous system (ENS) and the central nervous system (CNS) that are crucial for neurotransmission and neurological health. Metabolites such as short-chain fatty acids (SCFA), neurotransmitters, and neuromodulators from the gut microbiota influence behavior and brain function. This review focuses on the study related with gut bacteria, including Bifidobacterium infantis and Lactobacillus species, producing various metabolites in gut including bile acids, SCFA, histamine, and others to communicate with the brain or CNS. Dysbiosis can lead to neurological conditions such as anxiety, depression, PD, and AD. SCFAs from gut bacteria bind to the free fatty acid receptors of intestinal epithelial cells (IECs), affecting neurones and influencing neuroactivity. Gut bacteria also produce neurotransmitters that regulate growth hormone release through interactions with the CNS and endocrine systems. Brain signals interact directly with the pituitary and adrenal glands through the hypothalamic-pituitary-adrenal (HPA) axis, which in turn communicates with enteroendocrine cells (EECs). Investigating probiotics, prebiotics, and dietary changes could open new avenues for treatment for mental and neurological problems.
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Nutrition, cognition and chronic kidney disease: A comprehensive review of interactions and interventions.
BACKGROUND: Cognitive impairment is a prevalent complication in chronic kidney disease (CKD), ranging from mild deficits in early stages to more severe conditions, such as mild cognitive impairment and dementia in advanced stages. CKD patients exhibit reduced performance in memory, attention, language, visuospatial abilities and executive functions. RESULTS AND DISCUSSION: Contributing factors include uraemic toxins, structural brain changes, blood-brain barrier dysfunction, anaemia and comorbidities like diabetes mellitus. Malnutrition, affecting nearly half of CKD patients, exacerbates cognitive decline through inflammation, oxidative stress and protein-energy wasting. Nutritional deficiencies, particularly in protein, vitamin D, B vitamins, omega-3 fatty acids and antioxidants, are linked to impaired cognition. Emerging evidence highlights the role of the gut-brain axis, with gut-derived uraemic toxins and microbiome alterations contributing to cognitive dysfunction. Processed foods and microplastics further compound risks by promoting inflammation and neurotoxicity. Dialysis and kidney transplantation offer opportunities for cognitive recovery, though challenges remain, particularly in haemodialysis patients. Nutritional interventions, including tailored protein intake, micronutrient supplementation and dietary counselling, are critical for mitigating cognitive decline. Addressing CKD comorbidities, such as anaemia and diabetes through targeted nutritional and pharmacological strategies, improves outcomes. Integrating psychological and social support enhances quality of life, given the high prevalence of anxiety and depression in CKD patients. CONCLUSIONS: Future research should focus on personalized nutrition, gut microbiota modulation and routine cognitive assessments to optimise care. A holistic approach combining medical, nutritional and psychosocial strategies is essential for improving cognitive and overall health in CKD patients.
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Gut microbiota depletion affects nutritional and behavioral responses to activity-based anorexia model in a sex-dependent manner.
BACKGROUND & AIMS: In the last decade, the role of the microbiota-gut-brain axis in eating behavior and anxiety-depressive disorders has gained increasing attention. Although a gut microbiota dysbiosis has been reported in anorectic patients, its pathophysiological role remains poorly understood. Thus, we aimed to characterize the potential role of gut microbiota by evaluating the effects of its depletion in the Activity-Based Anorexia (ABA) mouse model both in male and female mice. METHODS: Male and female C57Bl/6 mice were submitted (ABA group) or not (CT group) to the ABA protocol, which combines access to a running wheel with a progressive limited food access. Gut microbiota was previously depleted or not by a cocktail of antibiotics (ATB) delivered by oral gavages. We monitored body composition, anxiety-like behavior, leptin and adiponectin plasma levels, hypothalamic and hippocampal neuropeptides mRNA levels, as well as dopamine (DRD) and serotonin (5HT1 and 4) receptors mRNA expression. RESULTS: In response to the ABA model, the body weight loss was less pronounced in ATB-treated ABA compared to untreated ABA, while food intake remained unaffected by ATB treatment. ATB-treated ABA exhibited increased fat mass and decreased lean mass compared to untreated ABA both in male and female mice, whereas but plasma adipokine concentrations were affected in a sex-dependent manner. Only male ABA mice showed a reduced anticipatory physical activity in response to ATB treatment. Similarly, anxiety-like behavior was mainly affected in ATB-treated ABA male mice compared to ATB-treated ABA female mice, which was associated with male-specific alterations of hypothalamic CRH mRNA and hippocampal DRD and 5-HT1A mRNA levels. CONCLUSIONS: Our study provides evidence that ATB-induced gut microbiota depletion triggers alterations of nutritional and behavioral responses to the activity-based anorexia model in a sex-dependent manner.
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Impact of chemotherapy on the association between fear of cancer recurrence and the gut microbiota in breast cancer survivors.
BACKGROUND: Dysfunctional processing of fear memory may be involved in the pathophysiology of fear of cancer recurrence (FCR), which is cited as the major unmet psychological need of cancer survivors. Emerging evidence has shown that the microbiota-gut-brain (MGB) axis affects depressive and anxiety disorders, and chemotherapy-associated psychological distress. We therefore hypothesized that the gut microbiota is associated with FCR in cancer survivors. METHODS: This cross-sectional study enrolled women diagnosed with invasive breast cancer who were not currently undergoing chemotherapy. Fecal samples were obtained to assess the gut microbiota. FCR grade was assessed using the Concerns About Recurrence Scale (CARS). RESULTS: Mean age of the participants (n = 126) was 58 years; 47% had stage I disease. Multiple regression analysis with adjustment for possible confounders showed that the relative abundance of the Bacteroides genus (beta = 0.180, p = 0.03) was significantly and directly associated with FCR. In the 57 participants with a history of chemotherapy, higher FCR was associated with lower microbial diversity (p = 0.04), lower relative abundance of Firmicutes (p = 0.03) and higher relative abundance of Bacteroidetes (p = 0.04) at the phylum level, and higher relative abundance of Bacteroides (p < 0.01) and lower relative abundance of Lachnospiraceae.g (p = 0.03) and Ruminococcus (p = 0.02) at the genus level. CONCLUSION: Our findings provide the first evidence of an association between the gut microbiota and FCR and suggest that chemotherapy-induced changes in gut microbiota can influence FCR. Further studies should examine the effects of the gut microbiota on FCR using a prospective design.
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Perspective: Gestational Tryptophan Fluctuation Altering Neuroembryogenesis and Psychosocial Development.
Tryptophan, as the sole precursor of serotonin, mainly derived from diets, is essential for neurodevelopment and immunomodulation. Gestational tryptophan fluctuation may account for the maternal-fetal transmission in determining neuroembryogenesis with long-lasting effects on psychological development. Personality disorders and social exclusion are related to psychosocial problems, leading to impaired social functioning. However, it is not clear how the fluctuation in mother-child transmission regulates the neuroendocrine development and gut microbiota composition in progeny due to that tryptophan metabolism in pregnant women is affected by multiple factors, such as diets (tryptophan-enriched or -depleted diet), emotional mental states (anxiety, depression), health status (hypertension, diabetes), and social support as well as stresses and management skills. Recently, we have developed a non-mammal model to rationalize those discrepancies without maternal effects. This perspective article outlines the possibility and verified the hypothesis in bully-victim research with this novel model: (1). Summarizes the effects of the maternal tryptophan administration on the neuroendocrine and microbial development in their offspring; (2). Highlights the inconsistency and limitations in studying the relationship between gestational tryptophan exposure and psychosocial development in humans and viviparous animals; and (3). Evidences that embryonic exposure to tryptophan and its metabolite modify bullying interactions in the chicken model. With the current pioneer researches on the biomechanisms underlying the bully-victim interaction, the perspective article provides novel insights for developing appropriate intervention strategies to prevent psychological disorders among individuals, especially those who experienced prenatal stress, by controlling dietary tryptophan and medication therapy during pregnancy.
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Efficacy and safety of fecal microbiota transplantation for the treatment of diseases other than Clostridium difficile infection: a systematic review and meta-analysis.
The intestinal microbiome has been identified as a key modifier for a variety of health conditions. Fecal Microbiota Transplantation (FMT) has emerged as a fast, safe, and effective means by which to modify the intestinal microbiome and potentially treat a variety of health conditions. Despite extensive research of FMT for CDI, there is a lack of clarity informed by systematic synthesis of data regarding the safety and efficacy of FMT for other health conditions. This systematic review used PRISMA guidelines and was prospectively registered with PROSPERO (CRD42018104243). In March 2020, a search of MEDLINE, EMBASE, and PsycINFO was conducted. We identified 26 eligible studies. A meta-analysis of FMT for active Ulcerative Colitis (UC) showed that FMT significantly improved rates of clinical remission (OR = 3.634, 95% CI = 1.940 to 6.808, I2 = 0%, p < .001), clinical response (OR = 2.634, 95% CI = 1.441 to 4.815, I2 = 33%, p = .002) and endoscopic remission (OR = 4.431, 95% CI = 1.901 to 10.324, I2 = 0%, p = .001). With respect to Irritable Bowel Syndrome, a meta-analysis showed no significant change in symptoms following FMT (p = .739). Hepatic disorders, metabolic syndrome, and antibiotic-resistant organisms were conditions with emerging data on FMT. Serious adverse events (AE) were more often reported in control group participants (n = 43) compared with FMT group participants (n = 26). There were similar rates of mild to moderate AE in both groups. Preliminary data suggest that FMT is a potentially safe, well-tolerated and efficacious treatment for certain conditions other than CDI, with evidence for active UC being the most compelling.
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Akkermansia muciniphila gavage alleviates depression-like behaviors in female A53T α-synuclein transgenic mice.
Parkinson's disease (PD) is characterized not only by progressive motor deficits but also by non-motor symptoms, such as depression, which often emerge during the prodromal stage and significantly impair quality of life. While Akkermansia muciniphila (AKK) has shown potential in modulating neuroinflammation, its specific role and underlying mechanisms in alleviating PD-associated non-motor symptoms remain unclear. In this study, we investigated the effects of AKK intervention in 16-month-old female A53T α-synuclein (α-syn) transgenic mice. Behavioral assessments revealed that oral administration of AKK significantly ameliorated depression-like behaviors, evidenced by reduced immobility in the forced swim test and increased sucrose preference, without affecting motor function, spatial memory, or gastrointestinal motility. Mechanistically, the intervention exhibited genotype-specific effects: AKK significantly increased plasma 5-HT levels in C57 mice. This increase was associated with an enrichment of Lactobacillus taiwanensis and metabolic pathways favoring peripheral tryptophan conversion. Conversely, in A53T mice, the treatment specifically elevated hippocampal 5-HT levels without altering plasma concentrations. This central effect correlated with distinct microbial remodeling, characterized by the enrichment of butyrate/propionate-producing Lachnospiraceae and the activation of purine degradation. Collectively, these findings provide novel mechanistic insights into the therapeutic potential of AKK for managing non-motor symptoms in PD. While limited to a female cohort, our results suggest that AKK ameliorates depression-like behaviors in PD through sex-specific remodeling of the gut microbiome and serotonergic signaling.