Although numerous studies have suggested that chronic stress is a major risk factor for major depressive disorder, the process by which stress causes depression is still not fully understood. Previously, we investigated glucocorticoids, which are stress response hormones that activate a synapse-weakening pathway. Therefore, we hypothesized that chronic stress may cause synaptic depression, which could reduce excitability related to emotions. Animals underwent chronic restraint stress (CRS), followed by basal synaptic transmission measurement in hippocampal slices to assess synaptic function. Drugs were infused into the ventral hippocampus via cannulation before behavioral tests, including forced swimming, tail suspension, and sucrose intake tests, which evaluated depressive-like behaviors and anhedonia. The field excitatory postsynaptic potentials (fEPSPs) are reduced by chronic restraint stress (CRS) in the ventral hippocampus. The ventral hippocampi of mice treated with CRS showed low levels of fEPSP after the forced swim test (FST). In the FST and tail suspension test, CRS-induced increases in immobility time were prevented by the acute inhibition of AMPAR internalization by Tat-GluA23y, which also prevented fEPSP reduction. Mice lacking caspase-3 exhibited resilience to CRS-induced increases in immobility time in the FST, as well as changes in the functionality of synaptic AMPAR. Finally, the caspase-3 inhibitor Z-DEVD-FMK rapidly blocked the CRS-induced increase in immobility time in the FST and the CRS-induced decrease in sucrose preference. These findings suggest that chronic stress-related behavioral changes may require caspase-3-dependent alterations in ventral hippocampal synapses.

While the COVID-19 pandemic disproportionately impacted Black American communities, there is a lack of empirical research examining mental health experiences during the COVID-19 pandemic among this population. This report examines the relationship between the COVID-19 pandemic and stress, depression, and anxiety among Black women. A cohort study with supplementary data was conducted among 45 Black American women with depressive symptoms participating in an ongoing randomized controlled trial of a mindfulness-based intervention (M-Body) at a Federally Qualified Health Center. Depressive symptoms, anxiety, and stress were measured at multiple time points before and during the COVID-19 pandemic. On average, anxiety [Pre-pandemic: 7.4 (0.5); Peri-pandemic: 7.0 (0.6); MD: -0.4 (0.5), p = 0.18] did not change substantially during the pandemic compared to pre-pandemic levels. However, depression [Pre-pandemic: 19.7 (1.4); Peri-pandemic: 24.4 (1.5); MD: 4.7 (1.0), p < 0.01] worsened while stress [Pre-pandemic: 21.7 (0.4); Peri-pandemic: 20.5 (0.5); MD: -1.2 (0.5), p = 0.01] slightly improved. Individuals caring for children exhibited modest but not statistically significant elevations in pre-pandemic stress than those who did not. These disparities more than doubled during the pandemic for stress [MD: 1.9 (0.9), p = 0.04] and depression [MD: 3.8 (2.6), p = 0.16] but increased only slightly for anxiety [MD: 1.8 (1.0), p = 0.08]. These data indicate that the COVID-19 pandemic impacted mental health among Black women with depressive symptoms, and those caring for children reported greater increases in depression, anxiety, and stress than those who did not during the pandemic. Trial Registration: ClinicalTrials.gov NCT03620721. Registered on 8 August 2018.

Chronic stress is a major contributor to the development of major depressive disorder, one of the leading causes of disability worldwide. Using a model of repeated social defeat stress in mice, we and others have reported that neuroinflammation plays a dynamic role in the development of behavioral deficits consistent with social avoidance and impaired reward responses. Animals susceptible to the model also exhibit hypomyelination in the medial prefrontal cortex, indicative of changes in the differentiation pathway of cells of the oligodendroglial lineage (OLN). We computationally confirmed the presence of immune oligodendrocytes, a population of OLN cells, which express immune markers and myelination deficits. In the current study, we report that microglia are necessary to induce expression of antigen presentation markers (and other immune markers) on oligodendroglia. We further associate the appearance of these markers with changes in the OLN and confirm that microglial changes precede OLN changes. Using co-cultures of microglia and OLN, we show that under inflammatory conditions the processes of phagocytosis and expression of MHCII are linked, suggesting potential priming for antigen presentation by OLN cells. Our findings provide insights into the nature of these OLN cells with immune capabilities, their obligatory interaction with microglia, and identify them as a potential cellular contributor to the pathological manifestations of psychosocial stress.

Chronic stress, a common risk factor for psychiatric disorders, is also implicated in the pathogenesis of Alzheimer's disease (AD). However, its underlying mechanisms remain elusive. Here, we provide evidence for chronic restraint stress (CRS), a widely used stress model in rodents, to regulate AD pathology. CRS not only induces prolonged depressive-like behaviors and cognitive deficits in young adult wild type (WT) mice, but also exacerbates a series of AD-related phenotypes in APP/PS1 mice, including impaired spatial learning and memory, increased β-amyloid plaques, promoted glial cells (astrocyte and microglial cell) activation and decreased dendritic spines in CA1 neurons. Single-nucleus RNA-sequencing analysis in hippocampus shows remarkable transcriptional changes in many cell type(s), and identifies oxidative phosphorylation pathway, a major source for adenosine triphosphate (ATP) production, is significantly downregulated in CA1 neurons by CRS stimuli. Furthermore, dysfunctional mitochondria and reduced ATP levels are also observed in CA1 neurons of CRS exposed WT and APP/PS1 mice. Interestingly, infusion of ATP in CA1 region abolishes the deficits in cognition, dendritic spines and glial activation in CRS exposed APP/PS1 mice. Taken together, these results uncover an unrecognized function of CA1 neurons in regulating CRS induced AD pathologies, and suggest ATP as a promising therapeutic strategy to improve brain health under stress condition.

Major depressive disorder (MDD) is a leading cause of disability that affects over 300 million people globally. Despite multiple antidepressant trials, approximately one-third of MDD patients remain symptomatic, progressing to treatment-resistant depression (TRD). This persistence possibly is due to the multifaceted etiology of TRD, encompassing biological, psychological, and environmental factors. Chronic stress, prevalent in modern life, significantly contributes to mental health disorders and complicates TRD treatment. This study investigated psilocybin as a potential TRD treatment using a diathesis-stress animal model. Twenty-two male Wistar-Kyoto (WKY) rats were divided into control and stress groups, with the stress group further subdivided to receive either sham treatment or psilocybin as early intervention. Behavioral assessments demonstrated a significant and sustained beneficial effect of psilocybin on behavioral despair and cognitive impairment. Biochemical analyses revealed psilocybin-induced increases in thyroid-stimulating hormone (TSH) levels without significant changes in the hypothalamic-pituitary-adrenal (HPA) axis. The ability of psilocybin to counter stress-induced TSH reductions suggested that TSH may serve as a proxy marker of therapeutic response, although its causal role in mood regulation remains unclear. Additionally, following psilocybin administration, changes in cannabinoid receptor type I (CB1R) suggest a potential modulation of psilocybin intervention on the component of the endocannabinoid system (ECS), though causal links remain unconfirmed without antagonist studies. These findings highlight the potential of psilocybin to treat TRD through the targeting of previously unexplored biological pathways.

The molecular mechanisms of chronic stress-induced psychiatric disorders, including depression, remain unknown. The current study aimed to assess the role of Cav3.1 T-type calcium channels as a gateway for the chronic stress-induced activation of parvalbumin (PV)-positive gamma-aminobutyric acidergic (GABAergic) neurons in the medial prefrontal cortex (mPFC) of mice.

The function of the Cav3.1 T-type calcium channel in the mouse mPFC following chronic stress was investigated using behavioral tests, electrophysiological analyses, transcriptome analyses, and optogenetic approaches.

Cav3.1-knockout (Cav3.1-/-) mice were resistant to chronic stress-induced depressive-like behaviors induced by repeated forced-swimming test or tail-suspension test. Immunohistochemical analysis revealed that Cav3.1 was predominantly localized in PV-positive GABAergic neurons in the mPFC. Based on transcriptomic and electrophysiological analyses, the excitatory-inhibitory (E-I) balance was disrupted by the chronic stress-induced activation of PV-positive GABAergic neurons in the mPFC of wild-type (WT) mice, but not in that of Cav3.1-/- mice. Optogenetic control of PV-positive GABAergic neurons in the mPFC revealed that they played a pivotal role in depressive-like behaviors. The administration of TTA-A2, a selective T-type calcium channel antagonist, reduced chronic stress-induced depressive-like behaviors.

The Cav3.1 T-type calcium channel acts as a gateway for the activation of GABAergic neurons in the mPFC of mice, thereby eliciting chronic psychobiological stress responses.

In addition to nasal symptoms, allergic rhinitis (AR) has increasingly been reported to be associated with depression-like behaviors. Recent evidence suggests that neuroinflammation in the hypothalamus may cause these depressive symptoms in AR. However, the precise mechanisms and effective treatments remain to be elucidated. This study investigated the ameliorative effects of metformin on neuroinflammation in the hypothalamus, depressive-like behavior and the underlying molecular mechanisms of AR mice. Mice were administered ovalbumin (OVA) intranasally to induce allergic rhinitis and subsequently subjected to behavioral experiments to detect depressive-like behavior. The roles of the TRPV1/NLRP3 pathway in depression-like behaviors in AR were examined in vivo. Additionally, the mechanism of TRPV1/NLRP3-mediated neuroinflammation was investigated in vitro. Finally, metformin was utilized to explore its possible mechanisms and efficacy in treating depressive-like behavior in AR. AR mice exhibited significant depressive-like behavior, which was attenuated by metformin. The number of Iba-1+ microglia significantly increased in the hypothalamus of AR mice. The expression of NLRP3 was significantly upregulated in the hypothalamus, activating microglia. Metformin ameliorated the neuropsychiatric symptoms by reducing NLRP3 expression in the hypothalamus. Moreover, metformin inhibited LPS-induced upregulation of the TRPV1/NLRP3 signaling pathway in microglial cell line, an effect that can be reversed by the TRPV1-specific agonist capsaicin. Increased TRPV1 expression activates the NLRP3 inflammasome in hypothalamic microglia, promoting the pathological process of depressive-like behavior in AR mice. Metformin could effectively treat neuroinflammation by regulating microglia via TRPV1 downregulation, indicating its potential as a treatment for depressive-like behaviors in AR.

It is unclear how changes to the 2023-2024 Electronic Residency Application Service (ERAS) application will impact future applicants. We investigate students' perceptions about applying to residency during this transition period.

An anonymous electronic survey was sent to medical students through social media of a women's surgical society. Questions reflected aspects of the ERAS application.

There were 415 responses, with 68 ​% planning to apply into surgical specialties (SS) and 17 ​% into non-surgical specialties (NSS). Compared with the NSS group, SS students reported decreased confidence in successfully matching, less attainable applicant expectations, and increased personal sacrifices to pursue their residency of interest. Students interested in Plastic and Reconstructive Surgery (PRS) placed 3-times more importance on the number of publications than General Surgery students. Away rotations were rated significantly more important for Otolaryngology, Orthopaedic, and PRS students.

Students applying into surgical residencies experience unique stressors. Values among SS students differed across surgical subspecialties in preparation for the match. Further investigation characterizing the relationship between these values and characteristics of successful resident applicants is warranted.

Greenspace exposure is associated with lower depression risk. However, most studies have measured greenspace exposure using satellite-based vegetation indices, leading to potential exposure misclassification and limited policy relevance. We examined the association of street-view greenspace measures with incident depression in a prospective cohort of US women.

We applied deep learning segmentation models to 350 million US street-view images nationwide (2007-2020) to derive ground-level greenspace metrics, including percentage of trees, grass, and other greenspace (plants/flowers/fields), and linked metrics to Nurses' Health Study II participants' residences (N = 33,490) within 500 m each year. Cox proportional hazards models estimated the relationship between street-view greenspace metrics and incident depression, assessed through self-report of clinician-diagnosed depression or regular antidepressant use and adjusted for individual- and area-level factors.

In adjusted models, higher percentages of street-view trees were inversely associated with incident depression (HR per IQR, 0.98; 95%CI: 0.94-1.01) and specifically clinician-diagnosed depression (HR per IQR, 0.94; 95%CI: 0.90-0.99). Higher percentages of street-view grass were also inversely associated with incident depression, but only in areas with low particulate matter (PM2.5) levels (HR per IQR, 0.79; 95%CI: 0.71-0.86). Results were consistent after adjusting for additional spatial and behavioral factors, and persisted after adjusting for traditional satellite-based vegetation indices.

We observed participants who lived in areas with more trees visible in street-view images had a lower risk of depression. Our findings suggest tree-planting interventions may reduce depression risk.

Anxiety is a physiological, emotional response that anticipates distal threats. When kept under control, anxiety is a beneficial response, helping animals to maintain heightened attention in environments with potential dangers. However, an overestimation of potential threats can lead to an excessive expression of anxiety that, in humans, may evolve into anxiety disorders. Pharmacological treatments show variable efficacy among patients, highlighting the need for more efforts to better understand the pathogenesis of anxiety disorders. Mounting evidence suggests that astrocytes, a type of glial cells, are active partners of neurons in brain circuits and in the regulation of behaviors under both physiological and pathological conditions. In this review, I summarize the current literature on the role of astrocytes from different brain regions in modulating anxious states, with the goal of exploring novel cerebral mechanisms to identify potential innovative therapeutic targets for the treatment of anxiety disorders.

Background/Objectives: the COVID-19 pandemic accelerated the adoption of remote work, blurring the boundaries between professional and personal life. This shift resulted in longer working hours, negative emotional outcomes, and health issues, particularly among Generation Z employees. This study investigates the links between working overtime, tobacco dependence, night shifts, and chronic disease risk in Generation Z employees during the pandemic while also examining the roles of depression risk and health awareness. A quantitative research approach was used to administer a questionnaire and employ the chi-square test, t-test, and logistic regression analysis to compare overtime-related factors and chronic disease risks. Results: the overtime workers are 1.39 times more likely to develop chronic diseases than those who do not work overtime. The odds ratio (OR) for overtime workers is 1.41, indicating that working overtime is a major risk factor for chronic disease. Among overtime workers, tobacco dependence and depression risk are significantly correlated with the risk of chronic disease, while night shift work is not. Overtime workers' health awareness is significantly correlated with chronic disease risk and has a partial mediating effect on the relationship between tobacco dependence and chronic disease risk. This is due to the strong correlation (p < 0.001) between tobacco dependence and chronic disease, which limits the extent to which health consciousness can mitigate the negative effects of tobacco dependence. Conclusions: these findings highlight the importance of smoking cessation and mental health interventions in reducing the risk of chronic disease for Generation Z workers, particularly in the post-pandemic era.

There are large racial disparities in maternal health that cannot be explained by education, income, or other individual-level risk factors. This cross-sectional study estimated associations between racial inequity in police use of force at the community level and health outcomes of Black and White women.

Birth records were linked to maternal hospital discharge records and municipal police department data for 326,240 births occurring between January 1, 2012, and December 31, 2016, to Black and White women in the state of New Jersey. Outcomes, identified using diagnosis and procedure codes, were substance use (any/tobacco/alcohol/other), mental health disorders (any/depression/anxiety/other), asthma, obesity, hypertension (pre-existing/gestational), diabetes (pre-existing/gestational), severe maternal morbidity, other cardiovascular diseases, and preterm labor. Data were analyzed in 2024.

For Black women, living in a community with 1% greater racially-disproportionate police use of force was associated with higher odds of any mental health disorder (by 0.18%; 95% CI=0.08, 0.28), depression (0.19%; 95% CI=0.05, 0.33), anxiety (0.25%; 95% CI=0.09, 0.41), other mental health disorder (0.17%; 95% CI=0.07, 0.27), any substance use (0.26%; 95% CI=0.14, 0.38), tobacco use (0.31%; 95% CI=0.16, 0.46), other substance use (0.17%; 95% CI=0.04, 0.30), asthma (0.12%; 95% CI=0.04, 0.21), and preterm labor (0.17%; 95% CI=0.05, 0.29) in adjusted models. There were no robust associations with the other outcomes for Black women or with any of the outcomes for White women.

Racially-disproportionate police use of force was significantly associated with mental illness, substance use, asthma, and preterm labor of Black women. Results underscore the potential importance of institutionalized racism as a fundamental cause of health disparities.

Chronic stress exerts profound negative effects on cognitive and emotional behaviours and is a major risk factor for the development of neuropsychiatric disorders. However, the molecular links between chronic stress and its deleterious effects on neuronal and synaptic function remain elusive. Here, using a combination of in vitro and in vivo approaches, we demonstrate that the upregulation of miR-186-5p triggered by chronic stress may be a key mediator of such changes, leading to synaptic dysfunction. Our results show that the expression levels of miR-186-5p are increased both in the prefrontal cortex (PFC) of mice exposed to chronic stress and in cortical neurons chronically exposed to dexamethasone. Additionally, viral overexpression of miR-186-5p in the PFC of naïve mice induces anxiety- and depressive-like behaviours. The upregulation of miR-186-5p through prolonged glucocorticoid receptor activation in vitro, or in a mouse model of chronic stress, differentially affects glutamatergic and GABAergic synaptic transmission, causing an imbalance in excitation/inhibition that leads to altered neuronal network activity. At glutamatergic synapses, we observed both a reduction in synaptic AMPARs and synaptic transmission, whereas GABAergic synaptic transmission was strengthened. These changes could be rescued in vitro by a miR-186-5p inhibitor. Overall, our results establish a novel molecular link between chronic glucocorticoid receptor activation, the upregulation of miR-186-5p and the synaptic changes induced by chronic stress, that may be amenable to therapeutic intervention.

This systematic review summarizes evidence about perceived stress in adults with epilepsy to clarify the particularities and potential effects on the prognosis and consequences of the disease. This review follows the recommendations of the PRISMA statement and was registered in PROSPERO. Thirty-four articles were selected. In 89 % of the studies, stress in epilepsy was conceptualized as a process in which the demands of the environment exceed the organism's ability to cope. Stressful life events related to perceived stress in epilepsy included the COVID-19 pandemic and work-related problems. Perceived stress was identified as a seizure precipitant in 85 % of studies. In 67 % of studies, patients with epilepsy had higher perceived stress than healthy people. Female gender, youth, low educational levels, unemployment, poor social support, less than five years suffering the disorder, temporal lobe epilepsy, depression, poor seizure control, and polytherapy were identified as risk factors for increased stress. These studies highlight the need for the conceptualization of epilepsy within a chronic stress framework which could facilitate more appropriate clinical management.

Chronic stress is associated with promotion of inflammation and development of metabolic syndrome, as well as deterioration of diet quality. Inflammation can be modified by changes in dietary intake.

The aim of this study was to test the hypothesis that diet quality mediates the relationship of chronic stress with inflammation in patients with metabolic syndrome.

Participants with metabolic syndrome (n = 73, 62 ± 12 years old, 71% female) completed questionnaires on chronic stress (Perceived Stress Scale-10) and diet quality (Healthy Eating Index-2020). The Perceived Stress Scale-10 was dichotomized. The Healthy Eating Index-2020 score was used as a continuous variable, and higher scores indicate better diet quality. Inflammation was assessed using plasma high-sensitivity C-reactive protein (log-transformed). We used PROCESS in SPSS to test the hypothesis.

Patients in the higher stress group had lower Healthy Eating Index-2020 scores (worse diet quality) than those in the lower stress group (57 ± 13 vs 64 ± 10, P = .01). Diet quality mediated the relationship between chronic stress and inflammation (indirect effect, 0.211; 95% bootstrap confidence interval, 0.006-0.496). Higher stress was associated with lower diet quality (effect, -7.152; 95% confidence interval, -13.168 to -1.137) that was associated with increased inflammation (effect, -0.030; 95% confidence interval, -0.052 to -0.007).

Our findings show the important role of diet quality in the relationship of chronic stress with inflammation in patients with metabolic syndrome. Healthcare providers should encourage patients with higher stress to improve diet quality, which can decrease inflammation.

The study aims to explore the association between patients diagnosed with inflammatory bowel disease (IBD) in childhood or youth and mental health disorders.

The study is a register-based cohort study of patients with IBD-onset before 25 years of age and matched references. They were followed until 30 years of age. The incidence rate and incidence rate ratio (IRR) for a wide spectrum of mental health disorders were assessed based on diagnostic codes from the Danish National Patient Registry, reimbursed prescriptions for psychotropic medications, and composite measures combining diagnosis and medication. Furthermore, the relative excess risk due to interaction (RERI) for parental educational level and parental mental health disorders were estimated.

A total of 4904 patients with Crohn's disease (CD), 5794 with ulcerative colitis (UC), and 94,802 matched references were identified. Patients with CD-onset before age 18 had a higher risk of anxiety disorders (IRR 1.58 (CI95%: 1.33-1.86)), while patients with CD-onset between age 18 to 24 had a higher risk of both anxiety and mood disorders. Patients with UC-onset before age 18 had a higher risk of anxiety disorders (IRR: 1.39 (CI95%: 1.19-1.64)). In general, patients with IBD had a higher risk of receiving psychotropic medication. Parental education had a subadditive interaction with the risk of emotional disorders for both patients with CD and UC, while maternal mental health disorders had a subadditive interaction for patients with UC.

Patients with CD and UC have a higher risk of mental health disorders, primarily due to an elevated risk of emotional disorders and a higher use of psychotropic medication. Surprisingly, the study demonstrated subadditive effect of parental education and for patients with UC maternal mental health disorders on the risk of emotional disorders.

Chronic stress is a common trigger of multiple neuropsychiatric illnesses. Animal models are widely used to study stress-induced brain disorders and their interplay with neuroinflammation and other neuroimmune processes. Here, we apply the prolonged 12-week chronic unpredictable stress (PCUS) model to examine rat behavioral and hippocampal transcriptomic responses to stress and to chronic 4-week treatment with a classical antidepressant fluoxetine, an anti-inflammatory agent eicosapentaenoic acid (EPA), a pro-inflammatory agent lipopolysaccharide and their combinations. Overall, PCUS evoked anxiety-like behavioral phenotype in rats, corrected by chronic fluoxetine (alone or combined with other drugs), and EPA. PCUS also evoked pronounced transcriptomic responses in rat hippocampi, involving > 200 differentially expressed genes. While pharmacological manipulations did not affect hippocampal gene expression markedly, Gpr6, Drd2 and Adora2a were downregulated in stressed rats treated with fluoxetine, EPA and fluoxetine + EPA, suggesting their respective protein products (G protein-coupled receptor 6, dopamine D2 receptor and adenosine A2A receptor) as potential evolutionarily conserved targets under chronic stress. Overall, these findings support the validity of rat PCUS paradigm as a useful model to study stress-related anxiety pathogenesis, and call for further research probing how various conventional and novel drugs may (co)modulate behavioral and neurotranscriptomic biomarkers of chronic stress.

Repetitive transcranial magnetic stimulation (rTMS) is an emerging treatment for brain disorders, but its therapeutic mechanism is unknown. We developed a novel mouse model of rTMS with superior clinical face validity and investigated the neural mechanism by which accelerated intermittent theta burst stimulation (aiTBS) - the first rapid-acting rTMS antidepressant protocol - reversed chronic stress-induced behavioral deficits. Using fiber photometry, we showed that aiTBS drives distinct patterns of neural activity in intratelencephalic (IT) and pyramidal tract (PT) projecting neurons in dorsomedial prefrontal cortex (dmPFC). However, only IT neurons exhibited persistently increased activity during both aiTBS and subsequent depression-related behaviors. Similarly, aiTBS reversed stress-related loss of dendritic spines on IT, but not PT neurons, further demonstrating cell type-specific effects of stimulation. Finally, chemogenetic inhibition of dmPFC IT neurons during rTMS blocked the antidepressant-like behavioral effects of aiTBS. Thus, we demonstrate a prefrontal mechanism linking rapid aiTBS-driven therapeutic effects to cell type-specific circuit plasticity.

Detarium microcarpum Guill. & Perr. is used traditionally in Far North Cameroun to treat stomach aches, anxiety, epilepsy, and other mental disorders.

Evaluate the anxiolytic and antidepressant-like effects of D. microcarpum (DM) in unpredictable chronic mild stress (UCMS) model of depression in male rats and its impact on fecal enterobacteria of stressed rats.

Rats were handled daily (control) or subjected to the UCMS procedure for 42 days. Anxiety-like behaviors were assessed using the light and dark box test (LBD) and the open field test (OFT). Depressive-like behaviors were assessed using the forced swimming test (FST), the sucrose preference test (SPT), and the novelty suppressed feeding test (NSFT). Feces were then collected, followed by blood, brain, and duodenum sections after sacrifice. Monoamine levels, pro-inflammatory cytokines, oxidative stress factors, and nitrosative stress were assessed. Feces were introduced into Hectoen enteric agar for the identification of enterobacteria. An in vitro growth test was performed.

The DM ethanolic extract has significantly increased the time spent in the light box, in the LBD, and in the center area of the OFT. Moreover, the extract has significantly reduced the preference for sucrose in the SPT, the time of immobility in the FST, and the latency period to consume the pet in the NSFT. DM extract has significantly reduced serum cortisol levels. It also significantly decreased the pro-inflammatory cytokines TNF-α and Il-1β in both brain and duodenum homogenate. DM has increased the brain's serotonin, GABA, and dopamine levels. The DM extract also decreased the MDA and nitrite levels. It also increased the SOD and CAT activities in both brain and duodenal homogenate. Histologically, the DM extract restored the cell's density in hippocampi sections and prevented gut inflammation and peroxidation characterizing leaky gut syndrome. DM extract has no effect on the growth of enterobacteria species isolated in vitro.

The ethanolic extract of DM would have anxiolytic and antidepressant effects via the modulation of the HPA axis, brain antioxidant enzyme activities, inflammation, and nitrosative stress. Moreover, it could act by preventing leaky gut syndrome.

Transposable elements (TEs) are repetitive DNA sequences capable of being transcribed and reintegrated, or transposed, into distinct loci throughout the genome. While thought to be largely transcriptionally silenced in brain, TE transcription is increasingly recognized as dynamic and involved in human health and disease states, including in disorders of the brain. In this study, we annotated TE transcripts in publicly available RNA sequencing (RNAseq) of postmortem human brain tissue to investigate the expression profile of TE transcripts in individuals with Major Depressive Disorder (MDD) compared to healthy controls. Our findings reveal a robust and uniform downregulation of TE transcript expression in the brains of subjects with MDD relative to controls, this occurs most prominently in the orbitofrontal cortex (OFC) brain region, and MDD differentially impacts this TE expression by age and sex. This work points to the aberrant transcription of cortical TEs as a potentially overlooked molecular signature of MDD.

The long-tern implications of stress during university for individuals' mental health are not well understood so far. Hence, we aimed to examine the potential effect of stress while studying at university on depression in later life. We analysed data from two waves of the longitudinal Study on Occupational Allergy Risks. Using the 'work overload' and 'proving oneself' scales of the Trier Inventory for Chronic Stress and the Patient Health Questionnaire-2 (PHQ-2), participants reported chronic stress during university (2007-2009, mean age 22.2 years, T1) and depressive symptoms ten years later (2017-2018, mean age 31.6 years, T2). We performed linear regression analyses to explore the association between stress during university (T1) and later depressive symptoms (T2). Participants (N = 548, 59% female) indicated rather low levels of stress and depression (PHQ-2 mean score: 1.14 (range: 0-6)). We observed evidence for a linear association between overload at T1 and depression at T2 (regression coefficient (B) = 0.270; 95% confidence interval (CI) = 0.131 to 0.409; standardised regression coefficient (β) = 0.170). Our analyses yielded evidence for an association between chronic stress while studying and risk of depressive symptoms later in life. This finding underlines the importance of implementing sustainable preventive measures against stress among students.

Stress plays a key role in mental, neurological, endocrine, and immune disorders. The zebrafish (Danio rerio) is rapidly gaining popularity as s model organism in stress physiology and neuroscience research. Although the leopard (leo) fish are a common outbred zebrafish strain, their behavioral phenotypes and stress responses remain poorly characterized. Here, we examined the effects of a 5-week chronic unpredictable stress (CUS) exposure on adult leo zebrafish behavior, cortisol levels, and brain gene expression. Compared to their unstressed control leo counterparts, CUS-exposed fish showed paradoxically lower anxiety-like, but higher whole-body cortisol levels and altered expression of multiple pro- and anti-inflammatory brain genes. Taken together, these findings suggest that behavioral and physiological (endocrine and genomic) responses to CUS do differ across zebrafish strains. These findings add further complexity to systemic effects of chronic stress in vivo and also underscore the importance of considering the genetic background of zebrafish in stress research.

Chronic stress exerts profound effects on mental health, contributing to disorders such as depression, anxiety, and cognitive impairment. This study examines the potential of psilocybin to alleviate behavioral despair and cognitive deficits in a rodent model of chronic stress, focusing on the interplay between the Hypothalamic-Pituitary-Adrenal (HPA) axis and the Endocannabinoid System (ECS). Twenty-two male Wistar rats were divided into control and stress groups. Animals within the stress group were exposed to predator odor and chronic social instability to induce chronic stress, and were either sham treated, or given psilocybin. Behavioral assessments were conducted using the Open Field Test, Sucrose Preference Test, Novel Object Recognition, Elevated Plus Maze, and Forced Swimming Test to evaluate locomotion, anhedonia, memory, anxiety, and behavioral despair, respectively. Blood and brain samples were analyzed for biochemical markers. Results indicated that psilocybin significantly reduced stress-induced behavioral despair and cognitive impairments, likely through ECS-mediated downregulation of the HPA axis. These findings suggest that early intervention with psilocybin has sustained beneficial effects on stress-related behavioral and cognitive disturbances, underscoring its potential as a novel therapeutic approach for stress-related mental health disorders.

Nearly half of people report birth-related complications, which is thought to be a risk factor for postpartum depression (PPD).

The goal of this systematic narrative review and meta-analysis was to provide an updated examination of the literature linking specific maternal birth complications and PPD.

A systematic review was conducted focused on studies examining associations between specific maternal birth complications and PPD symptoms/and or diagnoses, along with meta-analyses to quantify the magnitude of associations for specific experiences. The review protocol was not pre-registered.

Searches were completed using PsycINFO and PubMed databases. We used four eligibility criteria: (a) article available in English, (b) study included a measure of dimensional or diagnostic depression, (c) include discrete experience of birth-related complication, and (d) included a statistical test of the bivariate association between depression in the postpartum period and a measure of birth-related complication. We excluded studies of newborn intensive care or infant health conditions, rather than maternal birth complications directly impacting the pregnant person's health. All analyses were conducted using Comprehensive Meta-Analysis Software. We considered patterns in sampling, measurement, and analytic designs. To address publication bias, we examined funnel plots and calculated Egger's test.

The review (61 studies; 1,853,282 total participants) revealed four categories of maternal birth complications (i.e., cesarean, preterm birth, pain, laceration). Both the narrative review and meta-analysis support positive associations between maternal birth complications overall and PPD symptoms and diagnoses (odds ratio, OR = 1.47, p < 0.001), with specific associations observed for cesarean deliveries (non-emergency: 1,792,725 participants; OR = 1.30, p < 0.001; emergency: 14,199 participants; OR = 1.48, p = 0.001), preterm birth (39,291 participants; OR = 1.97, p < 0.001), and pain (3,708 participants; OR = 1.75, p = 0.009). ORs were small-to-medium in magnitude. Laceration alone was not significantly associated with PPD (3,356 participants; OR = 1.18, p = 0.692).

This study expands upon previous research and provides nuanced perspective on the relationship between different types of maternal birth complications and PPD. This review was supported by a Ford Foundation Predoctoral Fellowship and 1F31MH135650-01.

This article examines the relationship between maternal exposure to adverse childhood experiences (ACEs), intimate partner violence (IPV), and two aspects of maternal mental well-being-stress and depressive symptoms in the context of Tirana, Albania. Data were obtained from a representative sample of 328 mothers of 2-3-year-old children, who were registered in Tirana's public nurseries. Findings show that maternal ACEs are positively associated with stress levels (β = .210, z = 4.03, p < .001) and depressive symptoms (β = .129, z = 2.62, p < .01). In addition, IPV partially mediates the effect of ACEs on maternal stress (β = .081, z = 3.75, p < .001) and fully mediates the effect of ACEs on depressive symptoms (β = .054, z = 2.87, p < .01). These results suggest that among mothers of toddlers in Tirana, ACEs influence stress levels both directly and via IPV, while they influence depressive symptoms only via IPV. The findings demonstrate long-term effects of maternal exposure to interpersonal violence on mental well-being.

Academic stress is a prevalent problem among university students, affecting both their psychological well-being and academic performance. This study aims to investigate the mediating roles of biological and psycho-behavioural variables in the relationship between academic stress and academic performance over the course of a semester. Through a longitudinal approach and using accessible data collection technologies, the results will enable the design of effective interventions to mitigate the impact of academic stress.

(i) Biological variables related to academic performance will mediate the relationship between academic stress and students' academic performance. (ii) Psycho-behavioural variables will also act as mediators in this relationship, impacting academic performance differently.

To explore the mediating roles of biological and psycho-behavioural variables in the relationship between academic stress and academic performance over the course of a university semester.

A longitudinal non-experimental observational design will be applied. Data will be collected in three assessment cycles, each consisting of three consecutive weeks during the academic semester.

A sample of 160 undergraduate students from the Faculty of Medicine of the University of Concepción will be included. Students will be recruited on a voluntary basis through social networks and student associations. Students under psychological or pharmacological treatment will also be included to more representatively reflect the student reality and to ensure the ecological validity of the study.

Participants will answer electronic questionnaires on academic stress and psycho-behavioural variables three times a week via the REDCap platform. In addition, smart devices will be used to continuously collect biological data such as heart rate, oxygen saturation, and sleep patterns. Students will also collect saliva samples three times a week to measure cortisol levels, and alpha-amylase enzyme activity.

(i) Descriptive analysis of variables will be performed using measures of central tendency and dispersion for continuous variables and frequencies and percentages for categorical variables. (ii) Bivariate and multivariate analyses will be conducted to compare groups. (iii) Random intercept cross-lagged models will be used to assess the direction and reciprocal effects between variables over time. To analyze mediations, structural models (SEM) will be applied, considering biological and psycho-behavioural variables as mediators.

It is anticipated that (i) biological variables, such as cortisol and salivary alpha-amylase, will play a significant mediating role in the relationship between academic stress and academic performance, particularly towards the end of the semester. (ii) psycho-behavioural variables will also have a mediating effect, with different impacts on academic performance depending on the level of stress experienced. The use of accessible technologies and non-invasive methods such as saliva sample collection will provide a replicable model for future research.

Chronic restrain stress (CRS) induces depression-like behaviors and demyelination in the brain; however, the relationship between these depression-like behaviors and demyelination remains unclear. Arketamine, the (R)-enantiomer of ketamine, has shown rapid antidepressant-like effects in CRS-exposed mice.

We examined whether arketamine can improve both depression-like behaviors and demyelination in the brains of CRS-exposed mice. Additionally, we investigated the role of transforming growth factor β1 (TGF-β1) in the beneficial effects of arketamine.

A single dose of arketamine (10 mg/kg) improved both depression-like behavior and demyelination in the corpus callosum of CRS-exposed mice. Correlations were found between depression-like behaviors and demyelination in this region. Furthermore, pretreatment with RepSox, an inhibitor of TGF-β1 receptor, significantly blocked the beneficial effects of arketamine on depression-like behaviors and demyelination in CRS-exposed mice. Finally, a single intranasal administration of TGF-β1 ameliorated both depression-like behaviors and demyelination in CRS-exposed mice.

The precise mechanisms by which TGF-β1 contributes to the effects of arketamine remain unclear.

These data suggest that CRS-induced demyelination in the corpus callosum may contribute to depression-like behaviors, and that arketamine can mitigate these changes through a TGF-β1-dependent mechanism.

Epigenetic modifications, including DNA methylation (DNAm), can play a role in the biological embedding of early-life adversity (ELA) through serotonergic mechanisms. The current study examines methylation of the CpG island in the promoter region of the stress-responsive serotonin transporter gene (SLC6A4) and is the first to jointly assess how it is influenced by ELA severity, timing, and type-specifically, deprivation and threat.

We use data from 627 Youth Emotion Project study participants, recruited from two US high schools. Using adjusted linear regressions, we analyze DNA collected in early adulthood from 410 participants and ELA based on interviewer-rated responses from concurrent Childhood Trauma Interviews, adjusting for survey-measured covariates.

ELA robustly predicted mean CpG island SLC6A4 DNAm percent across 71 CpG sites. Each additional major-severity ELA event was associated with a 0.121-percentage-point increase (p<0.001), equating to a 0.177 standard deviation (sd) higher DNAm level (95 % CI: 0.080, 0.274) with each 1-sd higher adversity score. When modeled separately, both childhood and adolescent ELA predicted SLC6A4 DNAm. When modeled jointly, adolescent ELA was most strongly predictive, and child adversity remained significantly associated with DNAm through indirect associations via adolescent adversity. Additionally, the ELA-SLC6A4 DNAm association may vary by adversity type. Across separate models for childhood and adolescent exposures, deprivation coefficients are positive and statistically significant. Meanwhile, threat coefficients are positive and not significantly significant but do not statistically differ from deprivation coefficients. In models including all ELA dimensions, one major adolescent deprivation event is associated with a 0.222-percentage-point increased SLC6A4 DNAm (p<0.05), or a 1-sd higher deprivation score with a 0.157-sd increased DNAm.

Results further implicate epigenetic modification on serotonergic neurotransmission via DNAm in the downstream sequelae of ELA-particularly adolescent deprivation-and support preventive interventions in adolescence to mitigate biological embedding.

Depression, the most prevailing mental health condition, remains untreated in over 30% of patients. This cluster presents with sub-clinical inflammation. Investigations trialling anti-inflammatory medications had mixed results. The lack of results may result from inflammation's complexity and targeting only a few of depression's abnormal pathways. Mind-body therapies' biological and neuro-imaging studies offer valuable insights into depression psychopathology. Interestingly, mind-body therapies, like yoga, reverse the aberrant pathways in depression. These aberrant pathways include decreased cognitive function, interoception, neuroplasticity, salience and default mode networks connectivity, parasympathetic tone, increased hypothalamic-pituitary-adrenal (HPA) axis activity, and metabolic hyper/hypofunction. Abundant evidence found yogic techniques improving self-reported depressive symptoms across various populations. Yoga may be more effective in treating depression in conjunction with pharmacological and cognitive therapies. Yoga's psychoneuroimmunology teaches us that reducing allostatic load is crucial in improving depressive symptoms. Mind-body therapies promote parasympathetic tone, downregulate the HPA axis, reduce inflammation and boost immunity. The reduced inflammation promotes neuroplasticity and, subsequently, neurogenesis. Improving interoception resolves the metabolic needs prediction error and restores homeostasis. Additionally, by improving functional connectivity within the salience network, they restore the dynamic switching between the default mode and central executive networks, reducing rumination and mind-wandering. Future investigations should engineer therapies targeting the mechanisms mentioned above. The creation of multi-disciplinary health teams offering a combination of pharmacological, gene, neurofeedback, behavioural, mind-body and psychological therapies may treat treatment-resistant depression.

Objective: This quasi-experimental research was to assess the effect of online traditional dance exercise program on stress among elderly in Nakhon Nayok province, Thailand. Methods: The elderly living in Nakhon Nayok province were recruited for the study. Multistage random sampling was employed to select participants. There is a total of 27 elderly people classified as experimental Group 15 people (received a 4-week online traditional dance exercise program) and control Group 12 people. Exercise data collected by the SPST20, pre- and postintervention testing was used to measure stress. An independent t-test analyses were performed to assess the effectiveness of program interventions. Results: After the program, there were statistically significant differences in mean scores of stress between the experimental and the control group. The level of stress of the elderly in the experimental group had decreased within and between groups after 4-week (p value < 0.05). Conclusion: Effectiveness of online traditional dance exercise program on the stress level of the elderly. It can reduce stress levels in the elderly. It could be applied with elderly in the community healthcare setting.

Evidence suggests a mind-body component to aging through which psychological distress from anxiety and depression drives molecular changes that promote early decline (ie, accelerated aging). Cancer survivors experience particularly high rates of anxiety and depression. Some survivors also have accelerated aging, though the relationships between anxiety and depression and aging are not clear. A synthesis of evidence is needed to understand the state of the science and impending priorities.

PubMed, Embase, CINAHL, Web of Science, and PsycNet databases were searched for studies that measured associations between depression, anxiety, and nonchronological aging in cancer survivors (2012-2022). Data were methodologically evaluated.

Survivorship studies were included if they were peer reviewed, published in English from 2012 to 2022, and measured associations between anxiety and depression and aging. In total, 51 studies were included. Just over half were cross-sectional (53%). Foci included functional (n = 35 [69%]) and biological (n = 16 [31%]). Functional aging measures included frailty, sarcopenia, geriatric assessment, and cognition. Biological aging measures included telomere length, telomerase, age-related inflammatory blood-based biomarkers, renal insufficiency, anemia, and DNA methylation. We tested 223 associations. Associations between anxiety, depression, and aging were generally positive, though with varying strengths. Most compelling were associations between functional aging and depression. There were concerns for selection and measurement biases.

Findings suggest positive associations between anxiety, depression, and aging among cancer survivors. Future work is needed to clarify temporality, develop a consensus on the measurement of aging, and diversify cohorts.

Difficulties in fear regulation can sometimes result in maladaptive fear responses. To better understand how to improve fear regulation, it is important to determine how known factors, such as sex hormone status and stress, might interact to influence fear memory. Research has shown that women with high estradiol levels (mid-cycle) and men exhibit better extinction retention compared to women with low estradiol levels (women in the early follicular cycle or using oral contraceptives). Stress has also been demonstrated to affect both the learning and retention of extinction. Despite documented interactions between stress and sex hormones, their combined effects have not been thoroughly studied. This study aims to examine the impact of stress as a function of sex hormone status on extinction learning and retention. A total of 168 non-clinical participants were studied, including men (n = 46), women using oral contraceptives (n = 38), women in the early follicular phase (n = 40), and women in mid-cycle (n = 44). On Day 1, fear acquisition training was performed. On day 2, prior to extinction training, half of the participants were exposed to a psychosocial stressor, while the other half performed a non-stressful control task. On day 3, extinction retention was tested. Fear was quantified using skin conductance responses, while stress hormones were quantified through saliva samples. Exposure to stress prior to extinction training did not affect extinction learning, regardless of sex hormone status. In contrast, pre-extinction stress exposure had different effects on extinction retention depending on hormone status. Stressed men showed impairment in extinction retention compared to controls, while the experimental condition had no effect on naturally cycling women. Regardless of stress exposure, early follicular women exhibited a deficit in fear regulation, while mid-cycle women showed effective fear regulation. Among women using oral contraceptives, the stress group demonstrated better extinction retention compared to the control group. These results demonstrate the importance of considering sex hormone status and stress exposure during extinction learning, as both components may modulate extinction retention. These results could help identifying hormonal conditions that may enhance the effectiveness of extinction-based psychological therapies used in the treatment of fear-related disorders.

Chronic stress has a profound impact on circadian regulation of physiology. In turn, disruption of circadian rhythms increases the risk of developing both psychiatric and metabolic disorders. To explore the role of chronic stress in modulating the links between neural and metabolic rhythms, we characterized the circadian transcriptional regulation across different brain regions and the liver as well as serum metabolomics in mice exposed to chronic social defeat stress, a validated model for studying depressive-like behaviors.

Male C57BL/6J mice underwent chronic social defeat stress, and subsequent social interaction screening identified distinct behavioral phenotypes associated with stress resilience and susceptibility. Stressed mice and their control littermates were sacrificed every 4 hours over the circadian cycle for comprehensive analyses of the circadian transcriptome in the hypothalamus, hippocampus, prefrontal cortex, and liver together with assessments of the circadian circulatory metabolome.

Our data demonstrate that stress adaptation was characterized by reprogramming of the brain as well as the hepatic circadian transcriptome. Stress resiliency was associated with an increase in cyclic transcription in the hypothalamus, hippocampus, and liver. Furthermore, cross-tissue analyses revealed that resilient mice had enhanced transcriptional coordination of circadian pathways between the brain and liver. Conversely, susceptibility to social stress resulted in a loss of cross-tissue coordination. Circadian serum metabolomic profiles corroborated the transcriptome data, highlighting that stress-resilient mice gained circadian rhythmicity of circulating metabolites, including bile acids and sphingomyelins.

This study reveals that resilience to stress is characterized by enhanced metabolic rhythms and circadian brain-liver transcriptional coordination.

Background: The COVID-19 pandemic has profoundly affected young adults' lives globally, including those in Germany. This study investigated mental health and quality of life during the pandemic, with a particular focus on mood. Immune fitness, the body's capacity to respond to health challenges (such as infections) by activating an appropriate immune response, was assessed as a physical health indicator. Methods: Data were collected from 317 participants, aged 18 to 35, via an online survey conducted between November 2021 and March 2022. Participants included 103 men (32.5%) and 214 women (67.5%), with a mean age of 25.5 years (SD = 4.1). Results: Compared to pre-pandemic levels, significant declines in mood, quality of life, immune fitness, and sleep quality were observed during the lockdown periods of the COVID-19 pandemic (p < 0.0125). The most pronounced effects were observed during the second lockdown, with declines extending into the second no-lockdown period for fatigue, depression, happiness, optimism, and immune fitness (p < 0.0125). Significant sex differences were found for the magnitude of mood effects (anxiety, depression, stress). No significant differences were found according to age or occupational status (student vs. work). Conclusions: The COVID-19 pandemic and associated lockdown periods had a significant negative effect on the mood, immune fitness, and well-being of young adults living in Germany.

Depression is emerging as a social and health-related issue worldwide. Rice bran possesses a variety of biological properties; however, its potential efficacy and molecular mechanisms in depression remain unclear. This study investigated the antidepressant effects of rice bran supplement (RBS) in a mouse model of chronic restraint stress (CRS)-induced depression. RBS was administered to mice subjected to CRS for 5 weeks. RBS improved depressive symptoms in CRS-exposed mice, as evidenced by increased sucrose preference and reduced immobility time. It reduced hypothalamic-pituitary-adrenal (HPA) axis-related hormones. Additionally, RBS downregulated the glucocorticoid receptor (GR) pathway and upregulated the ERK-CREB-BDNF pathway in the prefrontal cortex and hippocampus. Furthermore, RBS increased neurotransmitter levels and decreased monoamine oxidase levels in the brain. Molecular docking analysis indicated that γ-oryzanol (ORY) interacts with GR. Moreover, ORY inhibited GR activity in GR-transfected HEK293T cells. The effects of ORY were not significantly altered by treatment with GR antagonist mifepristone or GR siRNA, suggesting ORY functions as a GR antagonist. Additionally, ORY administration improved depressive behaviors in CRS-exposed mice and modulated the imbalance of HPA axis-related hormones in mice. Mechanisms of action in the RBS were partially attributed by ORY, a key component of RBS, suggesting that ORY contributes synergistically to the effect of RBS. Thus, RBS administration could be a promising therapeutic approach to treating CRS-induced depression.

Compromised mitochondrial electron transport chain (ETC) activities are associated with depression in humans and rodents. However, the effects of the enhancement of mitochondrial ETC activities on depression remain elusive. We recently reported that an extremely low-frequency electromagnetic field (ELF-EMF) of as low as 10 μT induced hormetic activation of mitochondrial ETC complexes in human/mouse cultured cells and mouse livers. Chronic social defeat stress (CSDS) for 10 consecutive days caused behavioral defects mimicking depression in mice, and using an ELF-EMF for two to six weeks ameliorated them. CSDS variably decreased the mitochondrial ETC proteins in the prefrontal cortex (PFC) in 10 days, which were increased by an ELF-EMF in six weeks. CSDS had no effect on the mitochondrial oxygen consumption rate in the PFC in 10 days, but using an ELF-EMF for six weeks enhanced it. CSDS inactivated SOD2 by enhancing its acetylation and increased lipid peroxidation in the PFC. In contrast, the ELF-EMF activated the Sirt3-FoxO3a-SOD2 pathway and suppressed lipid peroxidation. Furthermore, CSDS increased markers for mitophagy, which was suppressed by the ELF-EMF in six weeks. The ELF-EMF exerted beneficial hormetic effects on mitochondrial energy production, mitochondrial antioxidation, and mitochondrial dynamics in a mouse model of depression. We envisage that an ELF-EMF is a promising therapeutic option for depression.

We aimed to investigate the presence of common psychological factors (i.e., stress, depression, anxiety) and their impact on the Oral health-related quality of life (OHRQoL) in patients diagnosed with four oral mucosal diseases (OMDs): recurrent aphthous ulcers (RAU), oral lichen planus (OLP), oral leukoplakia (OLK), and oral submucous fibrosis (OSF).

A total of 229 patients with clinically diagnosed OMDs were enrolled in this study, consisting of 55 RAU, 68 OLK, 50 OLP, and 56 OSF patients. The patients were statistically analyzed for psychological problems and OHRQoL using the Visual Analog Scale (VAS)､ the 5-item Oral Health Impact Profile (OHIP-5) and the Depression Anxiety Stress Scale-21 (DASS-21) scales.

There were 229 valid questionnaires collected, consisting of 83 females and 146 males with a mean age of 45.24 (SD = 11.88) years. Multiple regressions between DASS-21 scores and OHIP-5 scores revealed generally negative impacts of psychological problems on OHRQoL, with depression on OLP (β = 0.47), OLK (β = 0.65) and OSF (β = 0.38), stress on RAU (β = 0.29), OLP (β = 0.72), OLK (β = 0.38) and OSF (β = 0.60), and anxiety on OLP (β = 0.33), OLK (β = 0.49) and OSF (β = 0.51).

Psychological problems like depression, stress, and anxiety were found to be prevalent in OMDs patients and adversely affected their OHRQoL. The results support the biopsychosocial medical model in the treatment of OMDs patients.

The present study reinforced the crucial roles of psychological factors in impacting OMDs patients' OHRQoL. Therefore, it is necessary to monitor patients' psychological status and OHRQoL using questionnaires like DASS-21 and OHIP-5. Followed by psychological interventions, the treatment is expected to be enhanced.

Although precarious employment (PE) has emerged as a growing public health concern, research on older adults is scarce. This study explored the associations between PE and the onset of depressive symptoms and problematic alcohol use among middle-aged and older workers. A total of 2536 Korean waged workers aged ≥45 years contributed 8486 observations from 2006 to 2022. PE was defined as a multidimensional construct that includes employment insecurity, income inadequacy, and a lack of worker rights and protection. Depressive symptoms and problematic alcohol use were assessed using the Center for Epidemiological Studies Depression Scale and the CAGE questionnaire. Generalized estimating equations were employed to determine the association of PE with depressive symptoms and problematic alcohol use after the two-year follow-up. Risk ratios (RR) and 95% confidence intervals (CI) were estimated. Women, individuals with older age and low educational background, and blue-collar workers were more likely to belong to the high PE group. For individual indicators of PE, daily employment (RR: 1.26, 95% CI: 1.05-1.53), the lowest wage quartile (RR: 1.32, 95% CI: 1.01-1.72), and lack of trade union (RR: 1.55, 95% CI: 1.10-2.17) were positively associated with depressive symptom onset in the follow-up. Compared with the group with the lowest overall PE, the group with the highest PE exhibited increased risks of experiencing the onset of depressive symptoms (RR: 1.62, 95% CI: 1.27-2.08) and problematic alcohol use (RR: 2.45, 95% CI: 1.16-5.17) in the follow-up. This study suggests that PE is a major social determinant of older workers' mental health.