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Dysbiotic drift: mental health, environmental grey space, and microbiota.
Advances in research concerning the mental health implications of dietary patterns and select nutrients have been remarkable. At the same time, there have been rapid increases in the understanding of the ways in which non-pathogenic microbes can potentially influence many aspects of human health, including those in the mental realm. Discussions of nutrition and microbiota are often overlapping. A separate, yet equally connected, avenue of research is that related to natural (for example, green space) and built environments, and in particular, how they are connected to human cognition and behaviors. It is argued here that in Western industrial nations a 'disparity of microbiota' might be expected among the socioeconomically disadvantaged, those whom face more profound environmental forces. Many of the environmental forces pushing against the vulnerable are at the neighborhood level. Matching the developing microbiome research with existing environmental justice research suggests that grey space may promote dysbiosis by default. In addition, the influence of Westernized lifestyle patterns, and the marketing forces that drive unhealthy behaviors in deprived communities, might allow dysbiosis to be the norm rather than the exception in those already at high risk of depression, subthreshold (subsyndromal) conditions, and subpar mental health. If microbiota are indeed at the intersection of nutrition, environmental health, and lifestyle medicine (as these avenues pertain to mental health), then perhaps the rapidly evolving gut-brain-microbiota conversation needs to operate through a wider lens. In contrast to the more narrowly defined psychobiotic, the term eco-psychotropic is introduced.
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The Ruminal Microbiome Alterations Associated with Diet-Induced Milk Fat Depression and Milk Fat Globule Size Reduction in Dairy Goats.
The aim of this study was to evaluate the effect of conjugated linoleic acid (CLA) on milk fat globule (MFG) size and the ruminal microbiome of goats. Twenty-four mid-lactation Saanen dairy goats weighing 49 ± 4.5 kg (168 ± 27 d in milk, 1.2 ± 0.1 kg milk/d, 2-3 years old) were randomly divided into four groups-a control (CON) group, which was fed a basal diet, and three CLA supplementation groups, in which 30 g CLA (low-dose group, L-CLA), 60 g CLA (medium-dose group, M-CLA), or 90 g CLA (high-dose group, H-CLA) was added to the basal diet daily. The experiment lasted for 21 days, during which time goat milk was collected for composition and MFG size analysis. On day 21 of feeding, ruminal fluid was collected from the CON and H-CLA groups for analysis of the changes in microorganismal abundance. The results showed that CLA supplementation did not affect milk production, milk protein, or lactose content in the dairy goats (p > 0.05), but significantly reduced the milk fat content (p < 0.01) compared with the CON group. The CLA supplementation significantly decreased the D[3,2] and D[4,3] of the MFGs in a dose-dependent manner (p < 0.01). Moreover, dietary CLA inclusion increased the proportion of small-sized MFGs and decreased that of large-sized ones. The results of 16S rRNA gene sequencing showed that CLA-induced milk fat depression in dairy goats was accompanied by significant changes in the relative abundance of ruminal bacterial populations, most of which belonged to the Firmicutes and Bacteroidetes phyla. The relative abundance of Rikenellaceae_RC9_gut_group and Prevolellaceae_UCG-003 in Bacteroidetes and UCG-002, Succiniclasticum, and norank_f__norank_o__Clostridia_vadinBB60_group in Firmicutes was significantly higher in the CON group than in the H-CLA group. In contrast, the relative abundance of norank_f__UCG-011, norank_f_Eubacterium_coprostanoligenes_group, unclassified_f__Lachnospiraceae, and UCG-001 in Firmicutes and norank_f__Muribaculaceae in Bacteroidetes was significantly higher in the H-CLA group than in the CON group. Correlation analysis showed that the milk fat content was negatively correlated with the relative abundance of some bacteria, including members of Firmicutes and Bacteroidetes. Similarly, MFG size (D[3,2] and D[4,3]) was negatively correlated with several members of Firmicutes and Bacteroidetes, including Lachnospiraceae, norank_f__UCG-011, UCG-001, norank_f__Eubacterium_coprostanoligenes_group (Firmicutes), and norank_f__Muribaculaceae (Bacteroidetes), while positively correlated with the relative abundance of some members of Firmicutes and Bacteroidetes, including Mycoplasma, Succiniclasticum, norank_f__norank_o__Clostridia_vadinBB60_group, UCG-002 (Firmicutes), and Rikenellaceae_RC9_gut_group (Bacteroidetes). Overall, our data indicated that CLA treatment affected milk fat content and MFG size in dairy goats, and these effects were correlated with the relative abundance of ruminal bacterial populations. These results provide the first evidence to explain the mechanism underlying diet-induced MFG from the perspective of the ruminal microbiome in dairy goats.
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Does the epithelial barrier hypothesis explain the increase in allergy, autoimmunity and other chronic conditions?
There has been a steep increase in allergic and autoimmune diseases, reaching epidemic proportions and now affecting more than one billion people worldwide. These diseases are more common in industrialized countries, and their prevalence continues to rise in developing countries in parallel to urbanization and industrialization. Intact skin and mucosal barriers are crucial for the maintenance of tissue homeostasis as they protect host tissues from infections, environmental toxins, pollutants and allergens. A defective epithelial barrier has been demonstrated in allergic and autoimmune conditions such as asthma, atopic dermatitis, allergic rhinitis, chronic rhinosinusitis, eosinophilic esophagitis, coeliac disease and inflammatory bowel disease. In addition, leakiness of the gut epithelium is also implicated in systemic autoimmune and metabolic conditions such as diabetes, obesity, multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis and autoimmune hepatitis. Finally, distant inflammatory responses due to a 'leaky gut' and microbiome changes are suspected in Alzheimer disease, Parkinson disease, chronic depression and autism spectrum disorders. This article introduces an extended 'epithelial barrier hypothesis', which proposes that the increase in epithelial barrier-damaging agents linked to industrialization, urbanization and modern life underlies the rise in allergic, autoimmune and other chronic conditions. Furthermore, it discusses how the immune responses to dysbiotic microbiota that cross the damaged barrier may be involved in the development of these diseases.
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The ENGAGE-2 study: Engaging self-regulation targets to understand the mechanisms of behavior change and improve mood and weight outcomes in a randomized controlled trial (Phase 2).
Despite evidence for effective integrated behavior therapy for treating comorbid obesity and depression, treatment response is highly variable and the underlying neurobiological mechanisms remain unknown. This hampers efforts to identify mechanistic targets in order to optimize treatment precision and potency. Funded within the NIH Science of Behavior Change (SOBC) Research Network, the 2-phased ENGAGE research project applies an experimental precision medicine approach to address this gap. The Phase 1 study focused on demonstrating technical feasibility, target engagement and potential neural mechanisms of responses to an integrated behavior therapy. This therapy combines a video-based behavioral weight loss program and problem-solving therapy for depression, with as-needed intensification of antidepressant medications, and its clinical effectiveness was demonstrated within a parent randomized clinical trial. Here, we describe the ENGAGE Phase 2 (ENGAGE-2) study protocol which builds on Phase 1 in 2 ways: (1) pilot testing of an motivational interviewing-enhanced, integrated behavior therapy in an independent, primarily minority patient sample, and (2) evaluation of a priori defined neural targets, specifically the negative affect (threat and sadness) circuits which demonstrated engagement and malleability in Phase 1, as mediators of therapeutic outcomes. Additionally, the Phase 2 study includes a conceptual and methodological extension to explore the role of microbiome-gut-brain and systemic immunological pathways in integrated behavioral treatment of obesity and depression. This protocol paper documents the conceptualization, design and the transdisciplinary methodologies in ENGAGE-2, which can inform future clinical and translational research in experimental precision medicine for behavior change and chronic disease management. Trial registration: ClinicalTrials.gov #NCT 03,841,682.
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Intestinal microbiota, probiotics and mental health: from Metchnikoff to modern advances: part III - convergence toward clinical trials.
Rapid scientific and technological advances have allowed for a more detailed understanding of the relevance of intestinal microbiota, and the entire body-wide microbiome, to human health and well-being. Rodent studies have provided suggestive evidence that probiotics (e.g. lactobacillus and bifidobacteria) can influence behavior. More importantly, emerging clinical studies indicate that the administration of beneficial microbes, via supplementation and/or fecal microbial transplant (FMT), can influence end-points related to mood state (glycemic control, oxidative status, uremic toxins), brain function (functional magnetic resonance imaging fMRI), and mental outlook (depression, anxiety). However, despite the advances in the area of gastro-biological psychiatry, it becomes clear that there remains an urgent need to explore the value of beneficial microbes in controlled clinical investigations. With the history explored in this series, it is fair to ask if we are now on the cusp of major clinical breakthroughs, or are we merely in the quicksand of Autointoxication II?
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Endometriosis, Pain, and Related Psychological Disorders: Unveiling the Interplay among the Microbiome, Inflammation, and Oxidative Stress as a Common Thread.
Endometriosis (EM), a chronic condition in endometrial tissue outside the uterus, affects around 10% of reproductive-age women, significantly affecting fertility. Its prevalence remains elusive due to the surgical confirmation needed for diagnosis. Manifesting with a range of symptoms, including dysmenorrhea, dyschezia, dysuria, dyspareunia, fatigue, and gastrointestinal discomfort, EM significantly impairs quality of life due to severe chronic pelvic pain (CPP). Psychological manifestations, notably depression and anxiety, frequently accompany the physical symptoms, with CPP serving as a key mediator. Pain stems from endometrial lesions, involving oxidative stress, neuroinflammation, angiogenesis, and sensitization processes. Microbial dysbiosis appears to be crucial in the inflammatory mechanisms underlying EM and associated CPP, as well as psychological symptoms. In this scenario, dietary interventions and nutritional supplements could help manage EM symptoms by targeting inflammation, oxidative stress, and the microbiome. Our manuscript starts by delving into the complex relationship between EM pain and psychological comorbidities. It subsequently addresses the emerging roles of the microbiome, inflammation, and oxidative stress as common links among these abovementioned conditions. Furthermore, the review explores how dietary and nutritional interventions may influence the composition and function of the microbiome, reduce inflammation and oxidative stress, alleviate pain, and potentially affect EM-associated psychological disorders.
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Maternal probiotic supplementation and effects on the fetal placenta.
Increasing number of pregnant women are consumi ng probiotics to promote their own health and that of their unborn fetuses. Such supplements are presumed to be safe for pregnant mothers and their unborn offspring. For pregnant mothers, such bioactive compounds might lower the risk of constipation, diarrhea, other gastrointestinal conditions, and pre-term birth, and prevent adverse pregnancy outcomes, including gestational diabetes mellitus and depression/anxiety. More research is needed to examine potential safety of probiotic consumption during pregnancy and long-term health consequences to offspring. The conceptus can also be indirectly affected by maternal probiotic supplementation through microorganism production of bioactive compounds. The placenta is in direct communication with the underlying uterine tissue. Thus, compounds in the maternal blood can easily transfer across the placenta and impact this hormonally sensitive organ. Select studies suggest that disruptions to the maternal microbiome dramatically affect the placenta. In the current review, we will therefore consider the evidence to date of how maternal probiotic supplementation affects the placenta. Three potential mechanisms we will explore include the possibility that maternal probiotic supplementation might impact the putative placenta microbiome. The second potential mechanism we will consider is that maternal probiotic consumption alters bacterial-derived metabolites, including short-chained fatty acids, polyamines, Vitamin B9, and Vitamin B12. The third potential mechanism to be discussed is that such supplements affect maternal and placental immune responses. Before probiotics are promoted for healthy pregnant women and those with gestational disorders, more studies, including those examining the effects on the placenta, are essential.
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Lower serum levels of IL-1β and IL-6 cytokines in adolescents with anorexia nervosa and their association with gut microbiota in a longitudinal study.
INTRODUCTION: Anorexia nervosa (AN) is an often chronic and debilitating psychiatric disease whose etiology is not completely understood. Recently, a potential role of inflammation has emerged in other psychiatric diseases, such as depression, PTSD and schizophrenia. The first results in adults with AN seemed to confirm a low-grade proinflammatory state until recent studies presented more differential findings. Studying adolescents with a shorter illness duration and fewer confounding factors might help elucidate the role of inflammation in the underlying pathophysiology of AN; however, the few available studies in adolescents remain ambiguous, and no longitudinal data are available in this age range. METHODS: We examined the proinflammatory cytokines Tumor Necrosis Factor-alpha (TNF-α), Interleukin (IL)-1β, IL-6, IL-15, and the cytokine-receptor IL-6 Receptor alpha (IL-6 Rα) in the serum of twenty-two hospitalized female adolescent patients with AN longitudinally at admission and discharge and compared their results to nineteen healthy controls (HC). We also collected clinical data and stool samples that were analyzed with 16S rRNA amplicon sequencing to explore potential influencing factors of cytokine changes. RESULTS: TNF-α serum levels were significantly elevated in patients with AN at admission, while IL-1β and IL-6 levels were lower at admission and discharge than in HC. After treatment, we also found significantly elevated levels of IL-6 Rα compared to HC, while IL-15 did not show significant changes. Exploratory analyses revealed positive associations of cytokine and genus-level changes between admission and discharge for IL-1β (Bacteroides) and IL-15 (Romboutsia), and negative associations for IL-15 (Anaerostipes) and TNF-α (uncultured Lachnospiraceae). CONCLUSION: We confirmed a previous finding of elevated levels of TNF-α also in adolescents with AN; however, the reduced IL-1β and IL-6 levels differed from the mostly increased levels found in adults. A mixed pro- and anti-inflammatory state appears to be present in adolescents, potentially due to their shorter illness duration. The gut microbiota, with its regulatory function on cytokine production, might play a role in mediating these inflammatory processes in AN and could offer targets for new therapeutic approaches.
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Microbial Dysbiosis as an Emerging Pathology of Suicidal Behaviour? A Critical Review, Passing Through Depression to Chronic Pain.
BACKGROUND: Suicidal behaviour (SB) is one of the most complex neuropsychiatric conditions, with an etiopathogenesis that remains elusive despite a myriad of studies revealing its multifaceted nature, influenced by various biological, psychological, socioeconomic and cultural factors, usually with complex reciprocal and synergistic interactions. Emerging evidence has recently suggested a potential involvement of pathogens and host-tissue derived microbial species in contributing to SB. This review aims to provide a concise synthesis of clinical evidence focusing on the presence of microbial alterations in subjects with SB and in those exhibiting risk factors for SB, thereby exploring a possible new perspective in suicidology. SUMMARY: We conducted a surveillance of the literature in the PUBMED database, from its inception to 10 May 2025, to identify associations between infection/microbial alterations with SB and some of its risk factors (by focusing on two pathologic examples of psychiatric and somatic origins, respectively: depression and chronic pain, two often closely related conditions). Major clinical findings were selected and synthesised into a hypothetical framework to support the presence of a microbe-related origin of SB. We found that SB was associated with selected infections, such as Toxoplasma gondii and Cytomegalovirus. Dysbiosis, including changes in diversity and/or abundance of selected microbial species, in the oral cavity, gastrointestinal tract, and other mucosal tissues, was observed in subjects with SB and individuals with psychiatric (depression) and somatic (chronic pain) risk factors of SB. KEY MESSAGE: Microbial dysbiosis might contribute to SB etiopathogenesis. Further studies in this emerging field of research are expected to provide additional mechanistic insights for an improved understanding, prevention, and therapeutic management of this neuropsychiatric condition.
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Advances in capsule-based fecal microbiota transplantation: clinical applications and innovations.
Capsule-based fecal microbiota transplantation (cFMT) has emerged as a vital tool for modulating gut dysbiosis for therapeutic intervention. This noninvasive alternative to traditional FMT avoids procedural invasiveness while offering logistical advantages in terms of storage, administration, and patient compliance. This review evaluates cFMT as a transformative approach across diverse diseases. Notably, cFMT demonstrates robust efficacy in restoring the microbial balance in Clostridioides difficile infection (CDI), inflammatory bowel disease (IBD), and multidrug-resistant infections, with outcomes comparable to those of conventional methods. It also alleviates symptoms and enhances microbiota diversity in small intestinal bacterial overgrowth (SIBO). However, the clinical benefits remain inconsistent for individuals with in irritable bowel syndrome (IBS) and functional constipation (FC), despite alterations in gut microbial diversity. Emerging applications highlight the potential of cFMT metabolic disorders (e.g., obesity and hypertension) via the modulation of gut-derived metabolites and neuropsychiatric conditions (e.g., depression and autism) through gut–brain axis signaling, in addition to chronic kidney disease and hepatic encephalopathy. Challenges such as donor variability, standardization gaps, and transient adverse effects hinder widespread adoption. Further advancements, including targeted colon-release formulations, synthetic microbial consortia, and single-cell delivery systems, could improve precision and scalability. Despite its transformative potential, the clinical adoption of cFMT hinges on rigorous quality control, mechanistic insights, and long-term safety data. In recent years, the United States Food and Drug Administration (FDA) has officially approved the oral microbiome therapy Vowst for marketing. This marked the gradual transition of fecal microbiota transplantation (FMT)-related therapies from clinical research to standardized clinical application, and at the same time, Vowst has become the world’s first oral fecal microbiome therapy approved by the FDA. This review highlights the role of cFMT in microbiota-targeted therapies while advocating for innovation to address current limitations and expand its therapeutic scope.