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Metabolic Dysfunction in Psychiatric Disorders: A Narrative Review of Shared Pathways Between Mental Illness and Cardiometabolic Disease.
Psychiatric disorders and cardiometabolic disease (CMD) frequently coexist and contribute to substantial morbidity, premature mortality, and reduced quality of life. Although this association is increasingly recognized, the shared biological and clinical pathways linking mental illness with metabolic dysfunction remain incompletely defined. This article is a narrative review that examines recent evidence on mechanisms connecting depression, anxiety, schizophrenia, severe mental illness (SMI), obesity, insulin resistance, diabetes, dyslipidemia, hypertension, and cardiovascular disease. A narrative review approach was used, with literature identified from major biomedical databases and prioritized according to relevance to shared psychiatric-metabolic mechanisms, clinical significance, recency, and methodological strength. The review focuses on chronic low-grade inflammation, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, insulin resistance, oxidative stress, mitochondrial dysfunction, altered brain energy metabolism, gut microbiome disruption, sleep and circadian disturbance, psychotropic medication effects, and behavioral and social determinants. Current evidence suggests that psychiatric and cardiometabolic disorders are associated through bidirectional and overlapping pathways rather than a single causal mechanism. Metabolic dysfunction may be associated with worsening psychiatric symptoms through inflammatory, neuroendocrine, and neurotrophic effects, while psychiatric illness may increase cardiometabolic risk (CMR) through stress biology, lifestyle factors, medication exposure, and fragmented healthcare access. Antipsychotic-associated weight gain and glucose-lipid abnormalities remain important, but metabolic changes may also precede long-term treatment exposure, particularly in psychotic disorders. These findings support routine metabolic screening, early risk stratification, individualized psychotropic prescribing, lifestyle intervention, and integrated care involving psychiatry, primary care, endocrinology, cardiology, nutrition, and behavioral health services. Future longitudinal studies and randomized trials are needed to clarify causality and evaluate interventions that improve both psychiatric and cardiometabolic outcomes. Metabolic health should be considered a core component of psychiatric assessment and management.
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Bifidobacteria modulate cognitive processes in an anxious mouse strain.
Increasing evidence suggests that a brain-gut-microbiome axis exists, which has the potential to play a major role in modulating behaviour. However, the role of this axis in cognition remains relatively unexplored. Probiotics, which are commensal bacteria offering potential health benefit, have been shown to decrease anxiety, depression and visceral pain-related behaviours. In this study, we investigate the potential of two Bifidobacteria strains to modulate cognitive processes and visceral pain sensitivity. Adult male BALB/c mice were fed daily for 11 weeks with B. longum 1714, B. breve 1205 or vehicle treatment. Starting at week 4, animals were behaviourally assessed in a battery of tests relevant to different aspects of cognition, as well as locomotor activity and visceral pain. In the object recognition test, B. longum 1714-fed mice discriminated between the two objects faster than all other groups and B. breve 1205-fed mice discriminated faster than vehicle animals. In the Barnes maze, B. longum 1714-treated mice made fewer errors than other groups, suggesting a better learning. In the fear conditioning, B. longum 1714-treated group also showed better learning and memory, yet presenting the same extinction learning profile as controls. None of the treatments affected visceral sensitivity. Altogether, these data suggest that B. longum 1714 had a positive impact on cognition and also that the effects of individual Bifidobacteria strains do not generalise across the species. Clinical validation of the effects of probiotics on cognition is now warranted.
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A genetic association study reveals the relationship between the oral microbiome and anxiety and depression symptoms.
BACKGROUND: Growing evidence supports that alterations in the gut microbiota play an essential role in the etiology of anxiety, depression, and other psychiatric disorders. However, the potential effect of oral microbiota on mental health has received little attention. METHODS: Using the latest genome-wide association study (GWAS) summary data of the oral microbiome, polygenic risk scores (PRSs) of 285 salivary microbiomes and 309 tongue dorsum microbiomes were conducted. Logistic and linear regression models were applied to evaluate the relationship between salivary-tongue dorsum microbiome interactions with anxiety and depression. Two-sample Mendelian randomization (MR) was utilized to compute the causal effects between the oral microbiome, anxiety, and depression. RESULTS: We observed significant salivary-tongue dorsum microbiome interactions related to anxiety and depression traits. Significantly, one common interaction was observed to be associated with both anxiety score and depression score, Centipeda periodontii SGB 224 × Granulicatella uSGB 3289 (P depressionscore = 1.41 × 10-8, P anxietyscore = 5.10 × 10-8). Furthermore, we detected causal effects between the oral microbiome and anxiety and depression. Importantly, we identified one salivary microbiome associated with both anxiety and depression in both the UKB database and the Finngen public database, Eggerthia (P IVW - majordepression - UKB = 2.99 × 10-6, P IVW - Self - reportedanxiety/panicattacks - UKB = 3.06 × 10-59, P IVW - depression - Finngen = 3.16 × 10 , - 16 P IVW - anxiety - Finngen = 1.14 × 10-115). CONCLUSION: This study systematically explored the relationship between the oral microbiome and anxiety and depression, which could help improve our understanding of disease pathogenesis and propose new diagnostic targets and early intervention strategies.
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Exploring the novel protein drug target BAG33339.1 of Porphyromonas gingivalis: an integrative subtractive proteomics and structural dynamics study.
Porphyromonas gingivalis, a gram-negative, bacterium interacts favourably with host subgingival biofilms to cause adult tooth decay and loss. Consequently, the host is infested with an uncontrollable microbial community and a compromised immune system, ultimately leading to tissue damage and bone resorption. P. gingivalis has also been known to cause cardiovascular and metabolic diseases, Alzheimer's disease, depression, prostate and digestive system cancer, rheumatoid arthritis, and adverse pregnancy outcomes with high detection frequencies. Rising concerns in the recent past, highlight the inefficiency of antibiotics and antiseptics in the treatment of P. gingivalis-related infections. Hence, the current scenario impels the discovery of an alternative therapeutic avenue against P. gingivalis-infections. To elucidate the unidentified bacterial mechanisms of infection, we screened a non-homolog of the host and gut microbiome as a novel druggable target from 173 essential hypothetical proteins of P.gingivalis (BAG33339.1). BAG33339.1 was an inner membrane protein with a hydrophobic N-terminal transmembrane helix and a primarily reconfiguring C-terminal helical region (Y36 to E52) while the residues (downstream of Lys45) lay in the disordered region. Frustration index coupled with the mutation matrix showed the steadiness of the transmembrane helix and dynamicity of the C-terminal residues finally yielding a 'U'-shaped protein conformation. The tendency of the disordered C-terminal residues was to generate P. gingivalis variants. The overall conformational stability was determined by equilibrating RMSD, Rg and SASA values corroborated by increasing H-bonds and helix settling. Targeting the ligand binding pockets of BAG33339.1 would guide future endeavours to tackle P. gingivalis interaction with host systems.
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Targeting the microbiome-gut-brain axis for improving cognition in schizophrenia and major mood disorders: A narrative review.
Cognitive impairment has been consistently found to be a core feature of serious mental illnesses such as schizophrenia and major mood disorders (major depression and bipolar disorder). In recent years, a great effort has been made in elucidating the biological causes of cognitive deficits and the search for new biomarkers of cognition. Microbiome and gut-brain axis (MGB) hormones have been postulated to be potential biomarkers of cognition in serious mental illnesses. The main aim of this review was to synthesize current evidence on the association of microbiome and gut-brain hormones on cognitive processes in schizophrenia and major mood disorders and the association of MGB hormones with stress and the immune system. Our review underscores the role of the MGB axis on cognitive aspects of serious mental illnesses with the potential use of agents targeting the gut microbiota as cognitive enhancers. However, the current evidence for clinical trials focused on the MGB axis as cognitive enhancers in these clinical populations is scarce. Future clinical trials using probiotics, prebiotics, antibiotics, or faecal microbiota transplantation need to consider potential mechanistic pathways such as the HPA axis, the immune system, or gut-brain axis hormones involved in appetite control and energy homeostasis.
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Clinical Chronobiology: Circadian Rhythms in Health and Disease.
Circadian rhythms (CRs) are entrainable endogenous rhythms that respond to external stimuli and regulate physiological functions. The suprachiasmatic nucleus (SCN) in the hypothalamus is the mammalian master clock that synchronizes all other tissue-specific peripheral clocks, primarily through gamma-aminobutyric acid (GABA) and vasoactive intestinal polypeptide (VIP). The SCN follows Earth's 24-hour cycle by light entrainment through the retinohypothalamic tract. At the cellular level, the core clock genes CLOCK, BMAL1, PER1-PER3, CRY1, and CRY2 regulate CRs in a negative feedback loop. The circadian disruption of the sleep-wake cycle manifests in at least six distinct clinical conditions. These are the circadian rhythm sleep-wake disorders (CRSWDs). Their diagnosis is made by history, sleep diaries, and actigraphy. Treatment involves a combination of timed light exposure, melatonin/melatonin agonists, and behavioral interventions. In addition, CR disturbances and subsequent misalignment can increase the risk of a variety of illnesses. These include infertility and menstrual irregularities as well as diabetes, obesity, fatty liver disease, and other metabolic syndromes. In addition, a disruption in the gut microbiome creates a proinflammatory environment. CR disturbances increase the risk for mood disorders, hence the utility of light-based therapies in depression. People with neurodegenerative disorders demonstrate significant disturbances in their CRs, and in their sleep-wake cycles. Circadian realignment therapies can also help decrease the symptomatic burden of these disorders. Certain epilepsy syndromes, such as juvenile myoclonic epilepsy (JME), have a circadian pattern of seizures. Circadian disturbances in epilepsy can be both the consequence and cause for breakthrough seizures. The immune system has its own CR. Disturbances in these due to shift work, for instance, can increase the risk of infections. CR disturbances can also increase the risk of cancer by impacting DNA repair, apoptosis, immune surveillance, and cell cycle regulation. Moreover, the timing of chemotherapeutic agents has been shown to increase their therapeutic impact in certain cancers.
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Human oral microbiome and its influence on mental health and brain disorders.
The human oral microbiome can affect brain functions directly through the trigeminal nerve and olfactory system and indirectly via the oral-gut-brain axis. However, the potential link between the oral microbiome and mental health remains an area that requires further investigation. Taking into consideration that gut microbiota dysbiosis plays a role in the onset and progression of several mental disorders, as well as the potential influence of the oral microbiome on mental health via direct pathways, the present narrative review explores the role of the human oral microbiome in health and disease, along with the factors that affect its composition, with a particular focus on its potential impact on mental health, including its involvement in a range of mental disorders and brain-related conditions, such as Alzheimer's disease, Parkinson's disease, autism spectrum disorder, anxiety, depression, stress, bipolar disorder, Down's syndrome, cerebral palsy, epilepsy, and schizophrenia. Chronic oral diseases can impair the oral mucosal barrier, allowing microorganisms and endotoxins to enter the bloodstream, triggering systemic inflammation, and affecting the blood-brain barrier. This pathway can lead to neuroinflammation and cognitive dysfunction and contribute to adverse mental health effects. Additionally, translocation of oral bacteria to the gut can drive persistent inflammation and thereby affect brain health. Multiple studies suggest a potential relationship between the oral microbiome and several mental disorders, but further research is needed to strengthen the evidence surrounding these associations and to fully clarify the underlying mechanisms linking the oral microbiome to these conditions. Given the promising implications, future research should focus on elucidating the biological mechanisms through which alterations in the oral microbiome influence the development and progression of determinate neurodegenerative and neuropsychiatric disorders. Additionally, identifying reliable biomarkers linked to the oral microbiome could enhance early detection, diagnosis, and monitoring of these conditions.
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Microbiome-driven precision psychiatry: integrating multi-omics, artificial intelligence, and personalized interventions along the gut-brain axis.
INTRODUCTION: This scoping review maps evidence for microbiome-driven precision psychiatry in depression and anxiety. METHODS: Following JBI guidance and PRISMA-ScR, we searched PubMed/MEDLINE and PubMed Central from inception to July 2026, supplemented by Google Scholar and backward citation searching. Human primary studies were screened and charted; findings were synthesized narratively. RESULTS: Of 58 identified records, 49 remained after deduplication, 35 full texts were assessed, and 28 studies were included. The evidence was predominantly observational. Taxonomic findings varied across populations, while studies of microbial functions, metabolites, multi-omics signatures, and treatment response suggested potential for biological stratification. Microbiome-targeted interventions and artificial intelligence models remain exploratory. DISCUSSION: Microbiome-derived biomarkers and predictive models require standardized methods, independent validation, and prospective evidence of clinical utility before routine psychiatric use.
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Nutritional Modulation of the Gut-Brain Axis: A Comprehensive Review of Dietary Interventions in Depression and Anxiety Management.
Mental health is an increasing topic of focus since more than 500 million people in the world suffer from depression and anxiety. In this multifactorial disorder, parameters such as inflammation, the state of the microbiota and, therefore, the patient's nutrition are receiving more attention. In addition, food products are the source of many essential ingredients involved in the regulation of mental processes, including amino acids, neurotransmitters, vitamins, and others. For this reason, this narrative review was carried out with the aim of analyzing the role of nutrition in depression and anxiety disorders. To reach the review aim, a critical review was conducted utilizing both primary sources, such as scientific publications and secondary sources, such as bibliographic indexes, web pages, and databases. The search was conducted in PsychINFO, MedLine (Pubmed), Cochrane (Wiley), Embase, and CinAhl. The results show a direct relationship between what we eat and the state of our nervous system. The gut-brain axis is a complex system in which the intestinal microbiota communicates directly with our nervous system and provides it with neurotransmitters for its proper functioning. An imbalance in our microbiota due to poor nutrition will cause an inflammatory response that, if sustained over time and together with other factors, can lead to disorders such as anxiety and depression. Changes in the functions of the microbiota-gut-brain axis have been linked to several mental disorders. It is believed that the modulation of the microbiome composition may be an effective strategy for a new treatment of these disorders. Modifications in nutritional behaviors and the use of ergogenic components are presented as important non-pharmacological interventions in anxiety and depression prevention and treatment. It is desirable that the choice of nutritional and probiotic treatment in individual patients be based on the results of appropriate biochemical and microbiological tests.
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Involvement of Microbiome Gut-Brain Axis in Neuroprotective Effect of Quercetin in Mouse Model of Repeated Mild Traumatic Brain Injury.
Repeated mild traumatic brain injury (rmTBI) poses adversity in the form of neurological deficits. The ignition of long-term neurological aberrations post-TBI is appended with the microbiota gut-brain axis perturbation. Herein, we examined whether quercetin, which is anti-inflammatory and antioxidant flavonoid, serves as a prebiotic and modifies the compromised microbiome gut-brain axis in rmTBI mouse model. Male C57BL/6 mice were subjected to rmTBI for 7 times. The quercetin (50 mg/kg) was administered peroral from the day1 of first injury till 7 days post-injury. The neurobehavioral assessments were performed using return of righting reflex (ROR), rotarod, forced swimming test (FST), elevated zero maze (EZM), novel object recognition test (NORT), and Y-maze. Mice fecal samples, brains, and intestines were collected for molecular studies. Mice underwent rmTBI showed significant neurological deficits in ROR and rotarod test and also exhibited long-term neuropsychiatric aberrations like anxiety- and depression-like phenotypes, and cognitive deficits in EZM, FST, and Y-maze assays, respectively. Repeated peroral administration of quercetin ameliorated these neuropsychiatric problems. Quercetin treatment also restored the increased expression of GFAP and decreased expression of occludin and doublecortin in the frontal cortex and hippocampus of rmTBI mice. The altered levels of acetate and propionate, and microbial phylum abundance in fecal samples were also normalized in the quercetin-treated group. We also noted an improved intestinal permeability indicated by reduced villi rupture, blunting, and mucosal thinning in quercetin-treated mice. We suggest that the neuroprotective effect of quercetin may be mediated via remodeling of the microbiome gut-brain axis in rmTBI mouse model.