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Red meat consumption in higher healthy eating index diets is associated with brain health critical nutritional adequacy, and fecal microbial diversity.
We evaluated whether red meat consumption, within diets of both high and low healthy eating index (HEI) quality, was associated with differences in brain health-critical micronutrient adequacy, mental health, diet quality, or fecal microbiota composition. Using data from 3643 adults in the American gut project, participants were stratified into four groups: high-HEI (≥ 80) with red meat (HH-R), high-HEI without red meat (HH-NR), low-HEI (< 80) with red meat (LH-R), and low-HEI without red meat (LH-NR). HH-R had higher protein intake and lower carbohydrate intake than HH-NR, with saturated fat levels within recommended limits. Brain health-critical micronutrient adequacies (selenium, vitamin B12, zinc, calcium, vitamin D3, choline) were significantly higher in HH-R (p < 0.001) than HH-NR. Higher HEI scores, irrespective of red meat consumption, were associated with reduced odds of depression (logOR = -2.22), PTSD (logOR = -3.80), and bipolar disorder (logOR = -5.90). Fecal microbiota diversity and richness were highest in HH-R, with higher Bacteroides caccae (padj = 0.003) and Clostridium hathewayi (padj < 0.001), while HH-NR showed higher Bifidobacterium adolescentis and Bacteroides eggerthii (padj < 0.001). Therefore, these findings suggest that the inclusion of red meat in a high-HEI diet improves brain health-supporting micronutrient adequacy without adverse effects on mental health or microbial diversity.
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Effects of inulin-derived difructose anhydrides on DSS-induced colitis-associated behavioral alterations and gut microbiota-related responses in mice.
Ulcerative colitis (UC) has shown a significant upward trend in global incidence and is frequently accompanied by psychiatric comorbidities such as anxiety and depression, severely impairing patients' quality of life. This study investigated the effects of inulin-derived difructose anhydride I (DFA-I) and difructose anhydride III (DFA-III) on dextran sulfate sodium (DSS)-induced UC-associated anxiety- and depression-like behavioral alterations in mice. Through oral administration, behavioral assessments, histopathology, cytokine analysis, gut microbiota sequencing, and short-chain fatty acid (SCFA) measurement, we evaluated the potential associations between DFA intervention and gut microbiota-gut-brain axis-related responses. The results suggested that DFAs, particularly 3% DFA-III, alleviated DSS-induced colonic injury and behavioral abnormalities, reduced serum levels of CORT, IL-6, and TNF-α, modulated hippocampal BDNF/p75NTR-related gene expression, and increased butyrate levels together with alterations in gut microbial composition. These findings provide preliminary evidence suggesting that inulin-derived DFAs may serve as potential prebiotic candidates for alleviating DSS-induced colitis-associated inflammatory and behavioral alterations.
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Regulating environmental arsenic-mediated gut-brain toxicity using chitosan-conjugated luteolin gold nanoparticles.
Anxiety and depression are two major contributors to global disease burden. Amongst various causal factors, exposure to even low doses of environmental heavy metals, like arsenic, can induce anxiety and depression-like behaviour in mammals. Ingestion of arsenic, primarily through contaminated drinking water, severely disrupts the gut microbes, thereby inducing structural and functional abnormalities in the brain. Fecal microbiota transplantation (FMT) from arsenic-exposed mice to recipient healthy mice (As-FMT) enriched LPS-secreting Gram-negative bacteria and upregulated the expression of TLR4 in intestinal epithelial cells. Consequently, inflammation, oxidative stress and compromised barrier integrity in the gut facilitated LPS translocation into the bloodstream and promoted systemic inflammation. The secretomes eventually affected the brain by activating microglia, altering neurotransmitter levels and reducing the glucocorticoid receptor (GR) expression, contributing to appearance of pyknotic nuclei in dentate gyrus of hippocampus and emergence of anxiety- and depression-like behaviour. Luteolin, a flavonoid, devoid of any apparent side-effects, yet known for its anti-inflammatory and antioxidant properties, showed potential in alleviating the gut-brain toxic effects. However, its limited solubility and bioavailability pose challenges for its effectiveness, for which chitosan-conjugated luteolin gold nanoparticles (CH-LuAuNPs) were synthesized. Interestingly, where FMT from arsenic-treated mice to healthy mice showed deleterious effects in the transplanted mice, FMT from arsenic-treated mice co-administered with CH-LuAuNP attenuated As-FMT-mediated disruption of the gut-brain axis. This study highlighted the critical contribution of healthy gut microbiota in preserving neurobehavioural physiology, as well as underscored the potential therapeutic benefits of luteolin nanoparticles in ameliorating arsenic-induced gut dysbiosis and consequent mental disorders.
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Maternal milk fat globule membrane enriched gut L. murinus and circulating SCFAs to improve placental efficiency and fetal development in intrauterine growth restricted mice model.
Intrauterine growth restriction (IUGR) caused by placental dysfunctions leads to fetal growth defects. Maternal microbiome and its metabolites have been reported to promote placental development. Milk fat globule membrane (MFGM) is known for its diverse bioactive functions, while the effects of gestational MFGM supplementation on the maternal gut microbiota, placental efficiency, and fetal development remained unclear. In this study, low protein diet-induced IUGR decreased the litter birth weight, fetal birth weight, and the fetal/placental ratio in pregnant mice, while gestational MFGM supplementation restored these impairments. Meanwhile, MFGM supplementation during gestation enriched intestinal Lactobacillus murinus (L. murinus) and increased luminal and circulating short chain fatty acids (SCFAs) in IUGR pregnant mice, which improved placental efficiency and fetal development due to an enhanced antioxidant capacity and a decreased inflammation. In addition, fecal microbiota transplantation (FMT) with MFGM-derived microbiota reprinted the promoted phenotypes of maternal litter characteristics, gut L. murinus enrichment, placental efficiency, and fetal gut development in MFGM-fed pregnant mice, which were also recapitulated by exogenous administration with L. murinus or SCFAs cocktail. Mechanically, MFGM, MFGM-derived microbiota, L. murinus, or SCFAs cocktail activated IUGR-induced depressive phosphorylation of PI3K-Akt signaling in the placenta. Moreover, in vitro placental cells cultivation under amino acid shortage model (AAS) or oxygen-glucose shortage model (OGS) was used to validate that MFGM-derived key microbial and circulating SCFAs cocktails can alleviate placental oxidative stress and inflammation via activating PI3K/Akt signaling. Taken together, gestational MFGM supplementation enriched intestinal L. murinus and circulating SCFAs of IUGR pregnant mice, thereby improving placental efficiency, fetal growth, and intestinal functions of IUGR fetus. Our findings will provide theoretical support for the application of MFGM in the maternal-placental-fetal nutrition to address pregnancy malnutrition-induced IUGR.
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ILSI Europe perspective review: site-specific microbiota changes during pregnancy associated with biological consequences and clinical outcomes: opportunities for probiotic interventions.
Pregnancy induces notable alterations in the gut, vaginal, and oral microbiota driven by hormonal, immune, metabolic, dietary, and environmental factors. During pregnancy, the gut microbiota is characterized by increased proportions of the genus Bifidobacterium and the phyla Pseudomonadota (formerly Proteobacteria) and Actinomycetota (formerly Actinobacteria). These changes occur alongside reduced alpha diversity and greater beta diversity, changes that influence maternal metabolism and fetal development. Shifts in gut and oral microbiota have been associated with complications such as preterm birth (PTB), pre-eclampsia, and gestational diabetes (GDM), though patterns are sometimes inconsistent. The vaginal microbiota remains Lactobacillus-dominant during pregnancy, with reduced diversity leading to reduced risk of pathogenic infection and increased diversity has been linked with a higher risk of PTB. Hormonal changes also affect the oral microbiota, potentially increasing pathogenic species and contributing to adverse outcomes like PTB. Probiotic supplementation during pregnancy has significant potential to reduce adverse pregnancy outcomes; however, clinical studies are still limited. Probiotics may be effective in alleviating maternal constipation and lead to lower PTB risk, particularly by modulating the vaginal microbiota, but they have limited impact on GDM. In the context of maternal mental health, some studies suggest benefits of probiotics in reducing anxiety, but effects on depression are inconclusive. This perspective examines how pregnancy-related microbial shifts, both natural and probiotic-induced, affect maternal and fetal health and highlights potential opportunities for the innovative use of probiotics during the gestation period.
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Spinal cord injury and gut microbiota: A review.
After spinal cord injury (SCI), intestinal dysfunction has a serious impact on physical and mental health, quality of life, and social participation. Recent data from rodent and human studies indicated that SCI causes gut dysbiosis. Remodeling gut microbiota could be beneficial for the recovery of intestinal function and motor function after SCI. However, few studies have explored SCI with focus on the gut microbiota and "microbiota-gut-brain" axis. In this review, the complications following SCI, including intestinal dysfunction, anxiety and depression, metabolic disorders, and neuropathic pain, are directly or indirectly related to gut dysbiosis, which may be mediated by "gut-brain" interactions. Furthermore, we discuss the research strategies that can be beneficial in this regard, including germ-free animals, fecal microbiota transplantation, probiotics, phages, and brain imaging techniques. The current microbial research has shifted from descriptive to mechanismal perspective, and future research using new technologies may further demonstrate the pathophysiological mechanism of association of SCI with gut microbiota, elucidate the mode of interaction of gut microbiota and hosts, and help develop personalized microbiota-targeted therapies and drugs based on microbiota or corresponding metabolites.
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Multi-Omics Advances in Major Depressive Disorder for Molecular Insights, Biomarker Discovery, and Therapeutic Development.
Major depressive disorder (MDD) affects hundreds of millions worldwide and remains a major unmet clinical need because conventional monoaminergic agents achieve remission in fewer than half of patients and leave a substantial treatment-resistant subgroup. To address this gap, integrative multi-omics approaches, combined with computational systems biology, are being used to dissect its multifactorial etiology. Here, we review key findings from large Genome-wide association studies (GWAS), single-cell and spatial transcriptomics, proteomics, and metabolomics that converge on disrupted neuroplasticity, immune-inflammatory signaling, HPA-axis dysregulation, mitochondrial metabolism, and gut-brain interactions. We describe how AI-driven network modeling and structure-based drug design (SBDD) are translating multi-omics signals into candidate biomarkers and mechanism-based therapeutics, for example, N-methyl-D-aspartate/glutamatergic modulators, kappa opioid antagonists, anti-inflammatory agents, and epigenetic modulators. We highlighted the clinical implications, specifically molecularly stratified biomarkers for patient selection, trial enrichment, and structure-guided optimization of rapid-acting antidepressants and microbiome-based interventions. Finally, we discuss the limitations and immediate translational priorities that emphasize the trajectory from multi-omics discovery to precision psychiatry for MDD.
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Effects of postweaning cadmium exposure on socioemotional behaviors in adolescent male mice.
Exposure to cadmium (Cd), a toxic heavy metal classified as an environmental endocrine disruptor, can exert significant toxicity in both animals and humans. However, the potential effects of Cd exposure on socioemotional behaviors are still poorly understood, as are the underlying mechanisms. In the present study, employing a series of behavioral tests as well as 16 S rRNA sequencing analysis, we investigated the long-term effects of Cd exposure on socioemotional behaviors and their associated mechanisms in mice based on the brain-gut interaction theory. The results showed that postweaning exposure to Cd reduced the ability to resist depression, decreased social interaction, subtly altered sexual preference, and changed the composition of the gut microbiota in male mice during adolescence. These findings provided direct evidence for the deleterious effects of exposure to Cd in the postweaning period on socioemotional behaviors later in adolescence, and suggested that these effects of Cd exposure may be linked to changes in the gut microbiota.
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[Review of traditional Chinese medicines in ameliorating neuropsychiatric diseases by improving the levels of monoamine neurotransmitters via gut microbiota regulation].
The degeneration of monoaminergic system and the reduction of monoamine neurotransmitters(MNTs) are associated with the occurrence of a variety of neuropsychiatric diseases, becoming the key indicators for clinical diagnosis and treatment. Recent studies suggested gut microbiota could influence the occurrence, development, and treatment of neuropsychiatric diseases by directly or indirectly regulating the synthesis and metabolism of MNTs. Rich clinical experience has been accumulated in the amelioration and treatment of neuropsychiatric diseases by traditional Chinese medicines. The traditional oral administration method demonstrates obvious advantages in regulating gut microbiota. It provides a new idea for explaining the pharmacodynamic material basis and mechanism of traditional Chinese medicines in ameliorating neuropsychiatric disease by improving the levels of MNTs via gut microbiota regulation. Focusing on three common neuropsychiatric diseases including Alzheimer's disease, Parkinson's disease, and major depression, we summarized the pathways of gut microbiota in regulating the levels of MNTs and the paradigms of traditional Chinese medicines in ameliorating neuropsychiatric diseases via the "bacteria-gut-brain axis", aiming to provide ideas for the development of drugs and treatment schemes.
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Gut Microbial Control of Neurotransmitters and Their Relation to Neurological Disorders: A Comprehensive Review.
The study explores the vital role of gut microbiota in regulating neurotransmitters and its subsequent effects on brain function and mental health. It aims to unravel the mechanisms by which microbial metabolites influence neurotransmitter synthesis and signaling. The ultimate goal is to identify potential therapeutic strategies targeting gut microbiota for the management and treatment of neurological disorders, such as depression, autism spectrum disorder (ASD), anxiety, and Parkinson's disease. The review synthesizes current research on the gut-brain axis, focusing on the influence of gut microbial metabolites on key neurotransmitters, including dopamine, serotonin, and gamma-aminobutyric acid (GABA). It incorporates a multidisciplinary approach, linking microbiology, neurobiology, and clinical research. Each section presents an in-depth review of scientific studies, clinical trials, and emerging therapeutic strategies. The findings highlight the intricate interplay between gut microbiota and the central nervous system. Gut microbes significantly impact the synthesis and signaling of crucial neurotransmitters, which play a pivotal role in neurological health. Evidence supports the hypothesis that modulating gut microbiota can alter neurotransmitter output and alleviate symptoms associated with neurological disorders. Notable therapeutic potentials include microbiota-targeted interventions for managing depression, ASD, anxiety, and Parkinson's disease. This comprehensive analysis underscores the critical connection between gut microbiota and neurological health. By bridging gaps between microbiology, neurobiology, and clinical practice, the study opens avenues for innovative therapeutic approaches. It provides a valuable resource for researchers, clinicians, and students, emphasizing the need for continued investigation into gut microbiota's role in neurological disorders and its therapeutic potential.