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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.
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The microbiome as a key regulator of brain, behavior and immunity: Commentary on the 2017 named series.
The focus on the microbiome for the 2017 Named Series in Brain, Behavior, and Immunity reflects the rapidly growing interest in commensal microbes and the effects that they can have on physiological processes often studied in PsychoNeuroImmunology Research. The studies included in this Named Series show that commensal microbes can impact immune system activity, as well as brain and behavioral processes across the lifespan, and are involved in behavioral and immunological responses to social stresses. The studies also show that dietary effects on brain, behavior, and immunity often involve alterations of the gut microbiota. Thus, diet can be used therapeutically for diseases and conditions involving the brain, behavior, and immunity, as can treatment with both pre- and probiotics. While this has been widely tested in animal models, fewer studies have focused on pre- and probiotic treatment in humans. The studies in this Named Series highlight the challenges of probiotic research in human populations, but also highlight the future promise of probiotics for human health. While emotional disorders, such as anxiety and depression have been often been linked to alterations in the gut microbiota, studies in this Named Series identify new domains involving interactions between the microbiota, brain, behavior, and immunity, including schizophrenia, traumatic brain injury, and stroke. As a whole, this collection of work demonstrates the importance of the microbiome in regulating key aspects of immunity, brain, and behavior, and provides important rationale for extending the work so that findings can be translated into clinical practice.
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Associations of body fat percentage-based obesity with depression and comorbidity-related gut microbiota features in college students.
INTRODUCTION: The association between body fat percentage (BFP)-defined obesity and depression in college students remains unclear, and gut microbiota alterations in this comorbid condition have not been fully characterized. METHODS: A total of 906 college students were recruited to examine the prevalence of comorbid obesity and depression and the association between body fat percentage-defined obesity and depression. Logistic regression was used for association analysis. Subsequently, 104 participants balanced for age and sex distributions across groups were selected and divided into four groups: obese with depression (G1), non-obese with depression (G2), obese without depression (G3), and non-obese without depression (G4). Fecal samples were analyzed by 16S rRNA gene sequencing. RESULTS: The prevalence of comorbid obesity and depression was 9.71%. BFP-defined obesity was significantly associated with depression after adjustment for covariates (OR = 1.62, 95% CI: 1.10-2.38). Gut microbiota analysis showed no significant differences in α-diversity among groups, whereas β-diversity differed significantly between the G1 and G4 (P < 0.05). Descriptive taxonomic profiles suggested differences in the relative abundances of several genera (e.g., decreased Akkermansia, increased Fusobacterium and Collinsella in G1). PICRUSt- based functional prediction suggested differences in inferred microbial metabolic pathways between G1 and other groups, including higher predicted lipopolysaccharide biosynthesis pathway abundance than in G2 and G4. DISCUSSION: BFP-defined obesity was associated with depression in college students. The microbiome findings were exploratory and suggest that co-occurring obesity and depression may be associated with differences in gut microbial composition and predicted functional potential. Larger longitudinal studies with direct functional and inflammatory measurements are needed.
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Understanding How Mental Health Influences IBD Outcomes: A Review of Potential Culprit Biological Mechanisms.
Inflammatory bowel disease (IBD) includes Crohn's disease (CD) and ulcerative colitis (UC). Similar to other chronic diseases, IBD is associated with negative mental health outcomes. The prevalence of anxiety and depression with IBD is increasing in western societies and there is a growing body of evidence suggesting a bidirectional relationship which remains poorly understood. This review seeks to distil current evidence on the epidemiology, biological mechanisms and microbial changes through which anxiety and depression may lead to worse IBD outcomes. The literature demonstrates that a prior diagnosis of depression is associated with an increased risk of developing IBD. Co-morbid anxiety or depression doubles the odds of adverse outcomes in IBD. Antidepressants appear to have class dependent effects on modulating disease activity in IBD with co-morbid depression. Chronic stress may drive IBD through a number of mechanisms, including inducing the hypothalamic pituitary axis, glucocorticoid resistance, increasing intestinal permeability, and releasing inflammatory cytokines. Alterations in the microbiome on either a genus or species' level has been shown to be affected by and have an impact on both mental health illness and IBD activity. Further research with high quality longitudinal follow-up data is required to clarify causal associations of anxiety/depression and IBD onset as well as measure the impact of different antidepressant classes and microbiome targeted strategies on disease progression and outcomes.
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Ultra-processed food exposure and adverse health outcomes: umbrella review of epidemiological meta-analyses.
OBJECTIVE: To evaluate the existing meta-analytic evidence of associations between exposure to ultra-processed foods, as defined by the Nova food classification system, and adverse health outcomes. DESIGN: Systematic umbrella review of existing meta-analyses. DATA SOURCES: MEDLINE, PsycINFO, Embase, and the Cochrane Database of Systematic Reviews, as well as manual searches of reference lists from 2009 to June 2023. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Systematic reviews and meta-analyses of cohort, case-control, and/or cross sectional study designs. To evaluate the credibility of evidence, pre-specified evidence classification criteria were applied, graded as convincing ("class I"), highly suggestive ("class II"), suggestive ("class III"), weak ("class IV"), or no evidence ("class V"). The quality of evidence was assessed using the GRADE (Grading of Recommendations, Assessment, Development, and Evaluations) framework, categorised as "high," "moderate," "low," or "very low" quality. RESULTS: The search identified 45 unique pooled analyses, including 13 dose-response associations and 32 non-dose-response associations (n=9 888 373). Overall, direct associations were found between exposure to ultra-processed foods and 32 (71%) health parameters spanning mortality, cancer, and mental, respiratory, cardiovascular, gastrointestinal, and metabolic health outcomes. Based on the pre-specified evidence classification criteria, convincing evidence (class I) supported direct associations between greater ultra-processed food exposure and higher risks of incident cardiovascular disease related mortality (risk ratio 1.50, 95% confidence interval 1.37 to 1.63; GRADE=very low) and type 2 diabetes (dose-response risk ratio 1.12, 1.11 to 1.13; moderate), as well as higher risks of prevalent anxiety outcomes (odds ratio 1.48, 1.37 to 1.59; low) and combined common mental disorder outcomes (odds ratio 1.53, 1.43 to 1.63; low). Highly suggestive (class II) evidence indicated that greater exposure to ultra-processed foods was directly associated with higher risks of incident all cause mortality (risk ratio 1.21, 1.15 to 1.27; low), heart disease related mortality (hazard ratio 1.66, 1.51 to 1.84; low), type 2 diabetes (odds ratio 1.40, 1.23 to 1.59; very low), and depressive outcomes (hazard ratio 1.22, 1.16 to 1.28; low), together with higher risks of prevalent adverse sleep related outcomes (odds ratio 1.41, 1.24 to 1.61; low), wheezing (risk ratio 1.40, 1.27 to 1.55; low), and obesity (odds ratio 1.55, 1.36 to 1.77; low). Of the remaining 34 pooled analyses, 21 were graded as suggestive or weak strength (class III-IV) and 13 were graded as no evidence (class V). Overall, using the GRADE framework, 22 pooled analyses were rated as low quality, with 19 rated as very low quality and four rated as moderate quality. CONCLUSIONS: Greater exposure to ultra-processed food was associated with a higher risk of adverse health outcomes, especially cardiometabolic, common mental disorder, and mortality outcomes. These findings provide a rationale to develop and evaluate the effectiveness of using population based and public health measures to target and reduce dietary exposure to ultra-processed foods for improved human health. They also inform and provide support for urgent mechanistic research. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42023412732.