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Polycystic ovary syndrome in 2025-insights and innovations.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age, with broad implications for reproductive, metabolic, cardiovascular, and psychological health. Antimüllerian hormone level has emerged as a unique biomarker reflecting both ovarian reserve and possibly playing a significant role as a neuroactive hormone in the pathogenesis of PCOS. Beyond reproductive concerns, PCOS confers an elevated lifetime risk of obesity, metabolic syndrome, and type 2 diabetes. With increasing evidence for the risk of myocardial infarction and stroke even in the reproductive years, PCOS is now considered a cardiovascular disease risk-enhancing factor. Novel insights into the alterations observed in the gut microbiome in PCOS suggest possible contributions to metabolic dysfunction and inflammation, opening avenues for innovative therapeutic strategies. Expanding on the gut-PCOS connection, the high prevalence of mental health disorders such as depression and anxiety observed in PCOS may be linked to gut dysbiosis. Although recent studies indicate differences in neuroimaging and cognitive function in women with PCOS compared with controls, rigorous evaluation accounting for other factors influencing cognition and longitudinal changes is needed. Given the increased prevalence of multisystem comorbidities, early diagnosis, especially in adolescence, will allow appropriate counseling and implementation of early prevention and frequent cardiometabolic screening. Together, these developments will ultimately allow for the development of novel therapies and result in comprehensive, patient-centered, and evidence-based care. Advances in understanding the pathogenesis of PCOS and its associated comorbidities and recognizing PCOS as a cardiovascular disorder risk-enhancing condition hold promise for improving long-term outcomes and quality of life for women living with PCOS.
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The microbiota-gut-brain axis and perceived stress in the perinatal period.
Perinatal perceived stress can contribute to worse health outcomes for the parent-child dyad. Given the emerging relationship between the microbiota-gut-brain axis and stress, this study sought to elucidate connections between bowel symptoms and the gut microbiome in relation to perceived stress at three time points in the perinatal period: two during pregnancy and one postpartum. Ninety-five pregnant individuals participated in a prospective cohort study from April 2017 to November 2019. Researchers assessed Perceived Stress Scale-10 (PSS); bowel symptoms (according to the IBS Questionnaire); psychiatrist assessment of new onset or exacerbated depression and anxiety; and fecal samples analyzed for alpha diversity (measures of gut microbiome diversity utilizing Shannon, Observed OTUs, and Faith's PD) at each timepoint. Covariates included weeks of gestation and weeks postpartum. PSS scores were divided into "Perceived Self-Efficacy" and "Perceived Helplessness." Increased gut microbial diversity was associated with decreased bowel symptoms, decreased overall perceived stress, increased ability to cope with adversity, and decreased distress in the postpartum period. This study found a significant association between a less diverse microbial community, lower self-efficacy early in pregnancy, and greater bowel symptoms and perceived helplessness later in the perinatal period, relationships that may ultimately point to novel diagnostic methods and interventions for perceived stress based on the microbiota-gut-brain axis.
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Existing and Future Strategies to Manipulate the Gut Microbiota With Diet as a Potential Adjuvant Treatment for Psychiatric Disorders.
Nutrition and diet quality play key roles in preventing and slowing cognitive decline and have been linked to multiple brain disorders. This review compiles available evidence from preclinical studies and clinical trials on the impact of nutrition and interventions regarding major psychiatric conditions and some neurological disorders. We emphasize the potential role of diet-related microbiome alterations in these effects and highlight commonalities between various brain disorders related to the microbiome. Despite numerous studies shedding light on these findings, there are still gaps in our understanding due to the limited availability of definitive human trial data firmly establishing a causal link between a specific diet and microbially mediated brain functions and symptoms. The positive impact of certain diets on the microbiome and cognitive function is frequently ascribed with the anti-inflammatory effects of certain microbial metabolites or a reduction of proinflammatory microbial products. We also critically review recent research on pro- and prebiotics and nondietary interventions, particularly fecal microbiota transplantation. The recent focus on diet in relation to brain disorders could lead to improved treatment outcomes with combined dietary, pharmacological, and behavioral interventions.
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Parkinson's disease and the gut microbiota connection: unveiling dysbiosis and exploring therapeutic horizons.
Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic neuronal loss, α-synuclein aggregation, and sustained neuroinflammation. Emerging evidence supports the gut-brain-microbiota axis as a pivotal player in the disease's pathogenesis. Dysbiosis, disruptions in the gut microbial composition, has been consistently observed in individuals with PD, with notable reductions in beneficial, short-chain fatty acid-producing bacteria and elevations in pro-inflammatory microbial species. These alterations contribute to increased intestinal permeability, systemic inflammation, and heightened neuroinflammatory responses that may drive α-synuclein misfolding and dopaminergic degeneration. In addition, microbial metabolites, including lipopolysaccharides and amyloid proteins such as curli, may promote neurodegeneration via immune and molecular mimicry pathways. Recent advances highlight the bidirectional influence of the microbiota-gut-brain axis on PD symptoms, ranging from motor deficits to non-motor features like constipation, depression, and cognitive decline. Several microbiota-modulating interventions, including probiotics, prebiotics, dietary strategies, antibiotics, and fecal microbiota transplantation, have demonstrated neuroprotective potential in both preclinical and clinical contexts. However, inter-individual variability, methodological heterogeneity, and the absence of longitudinal, multi-omics-integrated studies limit current understanding. The gut microbiome also holds promise as a non-invasive biomarker for early PD detection and prognosis, though standardization remains a challenge. Future research must clarify causal mechanisms, optimize therapeutic delivery, and integrate genetic, metabolic, and environmental data to advance precision medicine approaches. This review consolidates current knowledge on gut microbiota's role in PD pathophysiology and therapeutic innovation, providing a roadmap for future research directions.
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Prenatal Stress and Ethanol Exposure: Microbiota-Induced Immune Dysregulation and Psychiatric Risks.
Changes in maternal gut microbiota due to stress and/or ethanol exposure can have lasting effects on offspring's health, particularly regarding immunity, inflammation response, and susceptibility to psychiatric disorders. The literature search for this review was conducted using PubMed and Scopus, employing keywords and phrases related to maternal stress, ethanol exposure, gut microbiota, microbiome, gut-brain axis, diet, dysbiosis, progesterone, placenta, prenatal development, immunity, inflammation, and depression to identify relevant studies in both preclinical and human research. Only a limited number of reviews were included to support the arguments. The search encompassed studies from the 1990s to the present. This review begins by exploring the role of microbiota in modulating host health and disease. It then examines how disturbances in maternal microbiota can affect the offspring's immune system. The analysis continues by investigating the interplay between stress and dysbiosis, focusing on how prenatal maternal stress influences both maternal and offspring microbiota and its implications for susceptibility to depression. The review also considers the impact of ethanol consumption on gut dysbiosis, with an emphasis on the effects of prenatal ethanol exposure on both maternal and offspring microbiota. Finally, it is suggested that maternal gut microbiota dysbiosis may be significantly exacerbated by the combined effects of stress and ethanol exposure, leading to immune system dysfunction and chronic inflammation, which could increase the risk of depression in the offspring. These interactions underscore the potential for novel mental health interventions that address the gut-brain axis, especially in relation to maternal and offspring health.
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Polyphenols selectively reverse early-life stress-induced behavioural, neurochemical and microbiota changes in the rat.
There is a growing emphasis on the role of the microbiota-gut-brain axis as modulator of host behaviour and as therapeutic target for neuropsychiatric disorders. In addition, accumulating evidence suggests that early-life stress can exert long-lasting changes on the brain and microbiota, and this early adversity is associated with increased risk for developing depression in later life. The maternal separation (MS) model in rats is a robust paradigm to study the effects of early-life stress on the microbiota-gut-brain axis. Recently, we have shown that polyphenols, naturally occurring compounds associated with several health benefits, have anti-stress effects in in vitro models. In this study, we assess the therapeutic potential of a variety of both flavonoid and non-flavonoid polyphenols in reversing the impact of MS on behaviour and the microbiota-gut-brain axis. Rats underwent a dietary intervention with the naturally-derived polyphenols xanthohumol and quercetin, as well as with a phlorotannin extract for 8 weeks. Treatment with polyphenols prevented the depressive- and anxiety-like behaviours induced by MS, where xanthohumol effects were correlated with rescue of BDNF plasma levels. In addition, MS resulted in altered brain levels of 5-hydroxyindoleacetic acid (5-HIAA) and dopamine, accompanied by abnormal elevation of plasma corticosterone. Although polyphenols did not reverse neurotransmitter imbalance, xanthohumol normalised corticosterone levels in MS rats. Finally, we explored the impact of MS and polyphenolic diets on the gut microbiota. We observed profound changes in microbial composition and diversity produced by MS condition and by xanthohumol treatment. Moreover, functional prediction analysis revealed that MS results in altered enrichment of pathways associated with microbiota-brain interactions that are significantly reversed by xanthohumol treatment. These results suggest that naturally-derived polyphenols exert antidepressant-like effects in MS rats, which mechanisms could be potentially mediated by HPA regulation, BDNF levels rescue and modulation of the microbiota-gut-brain axis.
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A Systematic Review of the Effect of Probiotic Supplementation on Schizophrenia Symptoms.
BACKGROUND: Derangements of the gut microbiome have been linked to increased systemic inflammation and central nervous system disorders, including schizophrenia. This systematic review thus aimed to investigate the hypothesis that probiotic supplementation improves schizophrenia symptoms. METHODS: By using the keywords (probiotic OR gut OR microbiota OR microbiome OR yogurt OR yoghurt OR lactobacillus OR bifidobacterium) AND (schizophrenia OR psychosis), a preliminary search of the PubMed, Medline, Embase, Google Scholar, ClinicalTrials.gov, Clinical Trials Register of the Cochrane Collaboration Depression, Anxiety and Neurosis Group (CCDANTR), and Cochrane Field for Complementary Medicine databases yielded 329 papers published in English between January 1, 1960 and May 1, 2018. Attempts were made to search grey literature as well. RESULTS: Three clinical studies were reviewed, comparing the use of probiotics to placebo controls. Applying per-protocol analysis and a fixed-effects model, there was no significant difference in schizophrenia symptoms between the group that received probiotic supplementation and the placebo group post-intervention as the standardized mean difference was -0.0884 (95% CI -0.380 to 0.204, p = 0.551). Separate analyses were performed to investigate the effect of probiotic supplementation on positive or negative symptoms of schizophrenia alone. In both instances, no significant difference was observed as well. CONCLUSION: Based on current evidence, limited inferences can be made regarding the efficacy of probiotics in schizophrenia. Although probiotics may have other benefits, for example to regulate bowel movement and ameliorate the metabolic effects of antipsychotic medications, the clinical utility of probiotics in the treatment of schizophrenia patients remains to be validated by future clinical studies.
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Posttraumatic Stress Disorder: Does the Gut Microbiome Hold the Key?
Gut bacteria strongly influence our metabolic, endocrine, immune, and both peripheral and central nervous systems. Microbiota do this directly and indirectly through their components, shed and secreted, ranging from fermented and digested dietary and host products to functionally active neurotransmitters including serotonin, dopamine, and γ-aminobutyric acid. Depression has been associated with enhanced levels of proinflammatory biomarkers and abnormal responses to stress. Posttraumatic stress disorder (PTSD) appears to be marked in addition by low cortisol responses, and these factors seem to predict and predispose individuals to develop PTSD after a traumatic event. Dysregulation of the immune system and of the hypothalamic-pituitary-adrenal axis observed in PTSD may reflect prior trauma exposure, especially early in life. Early life, including the prenatal period, is a critical time in rodents, and may well be for humans, for the functional and structural development of the immune and nervous systems. These, in turn, are likely shaped and programmed by gut and possibly other bacteria. Recent experimental and clinical data converge on the hypothesis that imbalanced gut microbiota in early life may have long-lasting immune and other physiologic effects that make individuals more susceptible to develop PTSD after a traumatic event and contribute to the disorder. This suggests that it may be possible to target abnormalities in these systems by manipulation of certain gut bacterial communities directly through supplementation or indirectly by dietary and other novel approaches.
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FEATURE OF GUT MICROBIOTA IN PATIENTS WITH MIGRAINE AND HEALTHY INDIVIDUALS.
The gut - brain axis plays a significant role in the pathophysiology of migraine. This interaction can be influenced by multiple factors, such as gut microbiota profiles. The aim of the study was to analyze the gut microbiome state in patients with migraine and healthy individuals, to assess possible correlations between the detected changes in patients with migraine and the frequency, intensity of headaches, their psycho-emotional state, and quality of life. In total, 112 patients-16.3% of men and 83.7% of women. Subjects were divided into 2 groups depending on the presence of migraine: the main - patients with chronic and episodic forms of migraine, the control - healthy individuals. The study of the intestinal microbiome was performed by chromato-mass spectrometry. The following scales were used: Visual Analogue Scale/VAS, Migraine Disability Assessment/MIDAS, Back Depression Inventory/BDI. In patients with migraine compared with healthy individuals, significant changes were noted in the quantitative composition of certain resident microorganisms including Alcaligenes spp (p=0.0061), Clostridium coccoides (p=0.0021), Clostridium propionicum (p=0.0287), Eggerthella lenta (p=0.0138), Pseudonocardia spp (p=0.0210), and Rhodococcus spp (p=0.0164). The number of microscopic fungi such as Candida spp (p=0.0079), Micromycetes spp (p=0.0011) and Micromycetes spp (p=0.0010) were increased in patients with migraine compared to the control group. In the main group, a negative correlation was found between the level of 16 Alcaligenes spp and the score on the BDI score, HARS score (respectively: r= -0.6226, p= 0.007; r= -0.509, p=0.03), the frequency of attacks (r=-0.4879, p=0.046) and the VAS score (r=-0.487, p=0.046). Significant negative correlation was found between elevated level of Clostridium coccoides and MIDAS score (r=-0.5123, p=0.03), BDI score (r=-0.54, p=0.025) in the patients with migraine. At the same time, in the main group a positive correlation was detected between Eggerthella lenta level of and VAS score (r=0.4830, p=0.049). In the main group negative correlations were found between slightly increased content of endotoxin in the main group, the BDI score, HARS score (respectively: r=-0.697, p=0.001; r=-0.557, p=0.02) the frequency of attacks (r=-0.547, p=0.023), on the VAS score (r= -0.531, p=0.028), as well as MIDAS score (r =-0.556, p=0.02). The revealed peculiarities of gut microbiome changes in patients with migraines need further clarification in order to identify the possible role of the gut microbiome in the pathogenesis, clinical picture, and therapy of migraine, and is a promising area of further scientific research.
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Gut dysbiosis-influence on amygdala-based functional activity in patients with end stage renal disease: a preliminary study.
Patients with end-stage renal disease (ESRD) are notably accompanied by cognitive disorder and anxiety or depressive symptom. We aimed to explore the linkages of the amygdala-based MR parameters, cognitive and mood performance, systematic inflammation and gut microbiota in ESRD. This prospective study enrolled 28 ESRD patients (13 males and 15 females, mean age of 43.9 ± 13.8 years) and 19 age- and sex-matched healthy control (HC) (12 males and 7 females, mean age of 44.1 ± 10.0 years). All subjects underwent cognitive assessment, inflammatory factor and stool microbiota analysis, and brain MRI analysis [amygdala-based functional connectivity and voxel-based morphometry (VBM)]. ERSD was separated by different microbiota strains. All factors were compared between ESRD and HC, as well as between ESRD subgroups. Pearson correlation analysis and causal mediation analysis were conducted to further investigate the relationship among the factors derived from the gut microbiota, brain and systemic inflammation. ESRD displayed gut dysbiosis and increased systemic inflammation when compared to HC (all P < 0.05). Meanwhile, ESRD showed smaller VBM in amygdala, decreased functional connectivity in left amygdala - right inferior parietal lobe [P < 0.05, Gaussian Random Field (GRF) corrected] and worse cognitive or mood performance. Moreover, ESRD-B (Prevutella mainly), when compared to ESRD-A (Bacteroides mainly), displayed increased interleukin-6, self-rating anxiety scale and functional connectivity in left amygdala - bilateral anterior cingulate cortex / medial superior frontal cortex (P < 0.05, GRF corrected). Furthermore, the correlation network of ESRD showed that both gut dysbiosis and amygdala-based alteration were correlated with cognitive performance and systemic inflammation. Causal mediation analysis validated that the disrupted distribution of Roseburia indirectly regulated the amygdala-based functional connectivity through tumor necrosis factor-alpha. The gut dysbiosis induced by ESRD was closely related to pro-inflammatory cytokines, amygdala-based phenotype, and mood performance. The lower abundance in Roseburia indirectly modulated amygdala-based functional connectivity pattern by tumor necrosis factor-alpha, which might provide a new way in diagnosis and treatment in patients of ESRD with depressive/anxious mood.