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Sex Differences and Emerging New Risk Factors for Atherosclerosis and Its Thrombotic Complications.
Cardiovascular diseases (CVD) remain the world's leading cause of death and disability in both men and women, but with different prognostics and outcomes between sexes. Although the burden of CVD is generally related to the conventional risk factors, the relevance of non-traditional risk factors is increasingly being recognized to explain the so-called "residual risk". Men and women share many similarities regarding classical cardiovascular risk factors but have different disease pathophysiology, clinical presentations, prevalence, and outcomes of CVDs. How sex-specificities regarding the effects of non-traditional risk factors may contribute to the evolution of atherosclerosis and its clinical manifestations in males and females remain largely underanalyzed. The present review summarizes the current knowledge for sex differences in atherosclerotic plaque composition and clinical evolution in association with risk factors, such as inflammation, lipoprotein(a), hemostasis, intraplaque calcification, and depression. We further discuss the potential sex-differential impact of chronic infectious diseases, gut microbiome and, epigenetic gene expression regulation for atherosclerosis and the effect of female-specific disorders in CVD.
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Capitalizing on the GLP-1 RA revolution for behavioral health through digital companions.
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Neuroimmune mechanisms of the gut-brain axis in treatment-resistant depression: Implications for microbiome-based therapeutic strategies.
Treatment-resistant depression (TRD) represents a major clinical challenge characterised by inadequate response to conventional antidepressant therapies and high relapse rates. Emerging evidence suggests that TRD may extend beyond monoaminergic dysfunction and may involve dysregulation of the HPA axis, neuroinflammation, impaired neuroplasticity, and disruption of the gut-brain axis (GBA). Gut dysbiosis has been associated with treatment resistance through alterations in monoamine turnover, immune signalling, intestinal barrier integrity, and drug-microbiome interactions affecting antidepressant bioavailability. This review integrates emerging evidence supporting targeted modulation of the GBA as a mechanistically informed strategy for TRD. Specific microbial strains (e.g., Christensenella minuta, Akkermansia muciniphila, Bifidobacterium breve CCFM1025), microbial metabolites (e.g., indole-3-propionic acid, indole-3-lactic acid, anserine), and phytochemicals (e.g., curcumin, matrine, salidroside) are discussed for their proposed roles in modulating neuroendocrine signalling, neuroinflammation, and synaptic plasticity. The review also highlights emerging peripheral biomarkers, including the kynurenine/tryptophan ratio, serum metabolomics, and lymphocyte serotonin transporter clustering, as candidate tools for stratified psychiatry. Most of the evidence discussed in this review comes from animal studies, in vitro systems, and computational analyses, while direct evidence in patients with treatment-resistant depression remains limited. These findings provide important mechanistic insights into gut-brain axis dysfunction but require further validation in human TRD populations. Biomarker-guided and endotype-based approaches targeting the gut-brain axis may offer a useful framework for future research, although their clinical utility has yet to be established.
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L. rhamnosus improves the immune response and tryptophan catabolism in laying hen pullets.
In mammals, early-life probiotic supplementation is a promising tool for preventing unfavourable, gut microbiome-related behavioural, immunological, and aromatic amino acid alterations later in life. In laying hens, feather-pecking behaviour is proposed to be a consequence of gut-brain axis dysregulation. Lactobacillus rhamnosus decreases stress-induced severe feather pecking in adult hens, but whether its effect in pullets is more robust is unknown. Consequently, we investigated whether early-life, oral supplementation with a single Lactobacillus rhamnosus strain can prevent stress-induced feather-pecking behaviour in chickens. To this end, we monitored both the short- and long-term effects of the probiotic supplement on behaviour and related physiological parameters. We hypothesized that L. rhamnosus would reduce pecking behaviour by modulating the biological pathways associated with this detrimental behaviour, namely aromatic amino acid turnover linked to neurotransmitter production and stress-related immune responses. We report that stress decreased the proportion of cytotoxic T cells in the tonsils (P = 0.047). Counteracting this T cell depression, birds receiving the L. rhamnosus supplementation significantly increased all T lymphocyte subset proportions (P < 0.05). Both phenotypic and genotypic feather peckers had lower plasma tryptophan concentrations compared to their non-pecking counterparts. The probiotic supplement caused a short-term increase in plasma tryptophan (P < 0.001) and the TRP:(PHE + TYR) ratio (P < 0.001). The administration of stressors did not significantly increase feather pecking in pullets, an observation consistent with the age-dependent onset of pecking behaviour. Despite minimal changes to behaviour, our data demonstrate the impact of L. rhamnosus supplementation on the immune system and the turnover of the serotonin precursor tryptophan. Our findings indicate that L. rhamnosus exerts a transient, beneficial effect on the immune response and tryptophan catabolism in pullets.
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Microbiome: A Potential Component in the Origin of Mental Disorders.
It is not surprising to find microbiome abnormalities present in psychiatric disorders such as depressive disorders, bipolar disorders, etc. Evolutionary pressure may provide an existential advantage to the host eukaryotic cells in that it survives in an extracellular environment containing non-self cells (e.g., bacteria). This phenomenon is both positive and negative, as with other intercellular processes. In this specific case, the phenomenal amount of information gained from combined bacterial genome could enhance communication between self and non-self cells. This can be coupled to both pathological processes and healthy ones. In this review, we chose to examine potential associated disorders that may be coupled to the microbiome, from the perspective of their bidirectional communication with eukaryotic cells in the gut. Cognition, being the newest neural networking functionality to evolve, consumes a good amount of organismic energy, 30% of which arises from the gut flora. Furthermore, the mammalian gut is highly innervated and has a highly developed immune component, reflecting brain complexity. The brain-gut axis uses similar molecular messengers as the brain, which affects bacterial processes as well. Thus, any modification of normal bacterial processes may manifest itself in altered behavior/cognition, originating from the gut. The origin of some disorders associated with this bidirectional communication may be harnessed to restore normal functioning.
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Fecal Microbiota Analysis in Patients Going through a Depressive Episode during Treatment in a Psychiatric Hospital Setting.
RATIONALE: There is a worldwide prevalence of generalized anxiety and major depressive disorders (MDD). Gut⁻brain axis dysfunction, antibacterial activity, and modulatory effects of antidepressants toward intestinal bacteria have been shown both in vitro and in vivo. OBJECTIVES: In this study, we aimed to investigate the effects of hospital stay, including escitalopram administration, on gut microbiota in patients with depressive episodes. METHODS: After admission to the hospital and 7-days washout from all medications the composition of fecal microbiota samples was evaluated at baseline (W0) and after 6 weeks (W6), using 16S rRNA sequencing. The study was conducted on 17 inpatients (52.9% females), who followed the same daily hospital routine, including a standard diet and received 5⁻20 mg daily doses of escitalopram. RESULTS: At the end of treatment (W6), no change was observed in the Chao1 index. However, Shannon (median (Q1⁻Q3): W0 2.78 (2.67⁻3.02) vs. W6 3.11 (2.80⁻3.30)), and inverse Simpson (median (Q1⁻Q3): W0 9.26 (7.26⁻13.76) vs. W6 12.13 (9.17⁻15.73)) indices increased significantly compared to baseline values (False Discovery Rate p (q) = 0.031 and q = 0.011, respectively). We also found that between-subject W0 Bray⁻Curtis dissimilarities were significantly higher than W0⁻W6 within-subject dissimilarities (median (Q1⁻Q3): 0.68 (0.56⁻0.77) vs. 0.38 (0.35⁻0.52), two sided Mann⁻Whitney test p < 0.00001. The within-subject dissimilarities did not depend on sex, age, BMI, illness duration and a daily dose of escitalopram. No significant differences between taxa levels, at the studied time points, were observed when adjusted for multiple hypotheses testing procedures. CONCLUSIONS: We conclude that a six-week treatment in a psychiatric hospital setting resulted in increased alpha biodiversity in fecal microbiota, however its causal relationship with patients' mental health was not proved. We have also found that individual microbiome stability was not affected by hospitalization.
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Antidepressive Effect of Natural Products and Their Derivatives Targeting BDNF-TrkB in Gut-Brain Axis.
Modern neurological approaches enable detailed studies on the pathophysiology and treatment of depression. An imbalance in the microbiota-gut-brain axis contributes to the pathogenesis of depression. This extensive review aimed to elucidate the antidepressive effects of brain-derived neurotrophic factor (BDNF)-targeting therapeutic natural products and their derivatives on the gut-brain axis. This information could facilitate the development of novel antidepressant drugs. BDNF is crucial for neuronal genesis, growth, differentiation, survival, plasticity, and synaptic transmission. Signaling via BDNF and its receptor tropomyosin receptor kinase B (TrkB) plays a vital role in the etiopathogenesis of depression and the therapeutic mechanism of antidepressants. This comprehensive review provides information to researchers and scientists for the identification of novel therapeutic approaches for neuropsychiatric disorders, especially depression and stress. Future research should aim to determine the possible causative role of BDNF-TrkB in the gut-brain axis in depression, which will require further animal and clinical research as well as the development of analytical approaches.
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Clinical trial: A Mediterranean diet is feasible and improves gastrointestinal and psychological symptoms in irritable bowel syndrome.
BACKGROUND: Diet is fundamental to the care of irritable bowel syndrome (IBS). However, some approaches are not appropriate for individuals experiencing psychological symptoms. AIMS: To assess feasibility of a Mediterranean diet in IBS and its impact on gastrointestinal and psychological symptoms. METHODS: We recruited adults with Rome IV IBS and mild or moderate anxiety and/or depressive symptoms to an unblinded 6-week randomised controlled trial. Patients were randomised to Mediterranean diet counselling or habitual diet. We collected gastrointestinal and psychological symptom data, dietary data and stool samples for metagenomic sequencing. RESULTS: We randomised 59 individuals (29 Mediterranean diet, 30 control); 48 completed the study. The Mediterranean Diet Adherence Screener score was higher in the Mediterranean diet group than controls at week 6 (7.5 [95% CI: 6.9-8.0] vs. 5.7 [5.2-6.3], p < 0.001), and there was a greater score increase than controls (2.1 [95% CI: 1.3-2.9] vs. 0.5 [95% CI: 0.1-1.0], p = 0.004), demonstrating Mediterranean diet feasibility. There was a greater proportion of gastrointestinal symptom responders in the Mediterranean diet group than controls (24/29, 83% vs. 11/30, 37%, p < 0.001) and depression responders (15/29, 52% vs. 6/30 20%, p = 0.015). There was no difference in FODMAP intake at week 6 (p = 0.51). Gastrointestinal adverse events were similar (p = 0.588). There were no differences in change in microbiome parameters between groups. CONCLUSIONS: A Mediterranean diet is feasible in IBS and leads to improvement in gastrointestinal and psychological symptoms. Although this study was unblinded, these findings together with the broader benefits of the Mediterranean diet, provide strong impetus for future research in IBS. Australia New Zealand Clinical Trials Registry: ACTRN12620001362987.
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Decoding the neurocircuitry of gut feelings: Region-specific microbiome-mediated brain alterations.
Research in the last decade has unveiled a crucial role for the trillions of microorganisms that reside in the gut in influencing host neurodevelopment across the lifespan via the microbiota-gut-brain axis. Studies have linked alterations in the composition, complexity, and diversity of the gut microbiota to changes in behaviour including abnormal social interactions, cognitive deficits, and anxiety- and depressive-like phenotypes. Moreover, the microbiota has been linked with neurodevelopmental, neuropsychiatric, and neurodegenerative disorders. Interestingly, there appears to be specific brain regions governing the neurocircuitry driving higher cognitive function that are susceptible to influence from manipulations to the host microbiome. This review will aim to elucidate the region-specific effects mediated by the gut microbiota, with a focus on translational animal models and some existing human neuroimaging data. Compelling preclinical evidence suggests disruption to normal microbiota-gut-brain signalling can have detrimental effects on the prefrontal cortex, amygdala, hippocampus, hypothalamus, and striatum. Furthermore, human neuroimaging studies have unveiled a role for the microbiota in mediating functional connectivity and structure of specific brain regions that can be traced back to neurocognition and behavioural output. Understanding these microbiota-mediated changes will aid in identifying unique therapeutic targets for treating neurological disorders associated with these regions.
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Changes in respiratory and gut microbiota in asthma and depression associate with disease markers.
Asthma is heterogeneous and frequently accompanied by depression, affecting disease mechanisms and management. Both asthma and depression have been associated with inflammation and microbiota alterations, but their combined impact on microbial compositions remains unclear. Our exploratory study analyzed lung and gut microbiota in patients with asthma and depression to identify associations between microbiota composition and disease markers. This cross-sectional study included 20 healthy controls, 20 patients with asthma, and 20 patients with asthma and comorbid depression. Participants underwent clinical characterization and assessment of asthma control, depression, anxiety, and perceived stress. Induced sputum and fecal samples were collected for microbiota analysis, and inflammatory cytokines were measured in serum and sputum. Microbial profiling was performed using 16S rRNA gene sequencing. Lung function and FeNO levels were comparable between all groups. Asthma control scores were lower, and psychological scores were significantly higher in patients with asthma and comorbid depression compared with asthma alone and controls. Despite similar alpha and beta diversity across groups, sputum and fecal microbiota, particularly of healthy controls and comorbid patients, significantly differed in genus-level taxonomic composition. Correlation analyses demonstrated associations between clinical and psychological parameters and microbial profiles, including a consistent negative correlation between psychological scores and Neisseria abundance in both sputum and fecal samples. Asthma with comorbid depression is associated with distinct alterations in respiratory and gut microbiota, including reduced Neisseria perflava abundance correlating with psychological symptom severity.IMPORTANCEAsthma and depression frequently coexist, yet the potential contribution of microbial alterations to this comorbidity remains poorly understood. Because both respiratory and gut microbiota have been implicated in immune regulation and disease pathophysiology, characterizing microbiota patterns associated with asthma and depression may provide new insights into the biological links between these conditions. In this exploratory study, we investigated respiratory and gut microbiota in individuals with asthma, with and without comorbid depression, and healthy controls. Genus-level community composition differed between groups, particularly between controls and patients with asthma and depression. Notably, reduced abundance of Neisseria perflava in sputum and fecal samples was consistently associated with greater psychological symptom severity. These findings suggest that asthma accompanied by depression is associated with distinct alterations in microbial communities at multiple body sites. Further studies are warranted to determine whether such microbiota-psychological associations contribute to disease mechanisms or may serve as biomarkers of asthma-depression comorbidity.