Chronic stress can result in various conditions, including psychological disorders, neurodegenerative diseases, and accelerated brain aging. Gut dysbiosis potentially contributes to stress-related brain disorders in individuals with chronic stress. However, the causal relationship and key factors between gut dysbiosis and brain disorders in chronic stress remain elusive, particularly under non-sterile conditions. Here, using a repeated restraint stress (RRS) rat model, we show that sequential transplantation of the cecal contents of different RRS stages to normal rats reproduced RRS-induced core phenotypes, including abnormal behaviors, increased peripheral blood corticosterone and inflammatory cytokines, and a unique gut microbial phenotype. This core phenotypic development was effectively inhibited with probiotic supplement. The RRS-induced unique gut microbial phenotypes at the genus level were positively or negatively associated with the levels of 20 plasma metabolites, including vitamin B6 metabolites 4-pyridoxic acid and 4-pyridoxate. Vitamin B6 supplement during RRS alleviated weight loss, abnormal behaviors, peripheral inflammation, and neuroinflammation, but did not affect the peripheral corticosterone levels in chronic stressed rats. Dampening inflammatory signaling via knocking out caspase 11 or caspase 1 inhibitor abolished RRS-induced abnormal behaviors and peripheral and neuroinflammation but did not decrease peripheral corticosterone in mice. These findings show that gut dysbiosis-induced vitamin B6 metabolism disorder is a new non-hypothalamic-pituitary-adrenal axis mechanism of chronic stress-related brain disorders. Both probiotics and vitamin B6 supplement have potential to be developed as therapeutic strategies for preventing and/or treating chronic stress-related illness.

Social relationships profoundly impact health in social species. Much of what we know regarding the impact of affiliative social relationships on health in nonhuman primates (NHPs) has focused on the structure of connections or the quality of relationships. These relationships are often quantified by comparing different types of affiliative behaviors (e.g., contact sitting, grooming, proximity) or pooling affiliative behaviors into an overall measure of affiliation. However, it is unclear how the breadth of affiliative behaviors (e.g., how many different types or which ones) a dyad engages in impact health and fitness outcomes. We used a novel social network approach to quantify the breadth of affiliative relationships based on two behaviors: grooming and sitting in contact. Dyadic relationships were filtered into separate networks depending on whether the pair engaged in multiple affiliative behaviors (multiplex networks) or just one (uniplex networks). Typically, in social network analysis, the edges in the network represent the presence of a single behavior (e.g., grooming) regardless of the presence or absence of other behaviors (e.g., contact sitting, proximity). Therefore, to validate this method, we first compared the overall structure of the standard network for each affiliative behavior: all grooming interactions regardless of contact sitting, and all contact sitting interactions regardless of grooming. We then similarly compared the structure of our filtered multiplex vs. uniplex networks. Results indicated that multiplex networks were more modular, reciprocal, and kin-based while connections in uniplex networks were more strongly associated with social status. These differences were not replicated when comparing networks based on a single behavior alone (i.e., all grooming networks vs. all contact sitting networks). Next, we evaluated whether individual network position in multiplex vs. uniplex (novel approach) or grooming vs. contact sitting (traditional approach) networks differentially impact inflammatory biomarkers in a commonly studied non-human primate model system, the rhesus macaque (Macaca mulatta). Being well connected in multiplex networks (networks where individuals both contact sat and groomed) was associated with lower inflammation (IL-6, TNF-alpha). In contrast, being well connected in uniplex grooming networks (dyad engaged only in grooming and not in contact sitting) was associated with greater inflammation. Altogether, these results suggest that multiplex relationships may function as supportive relationships (e.g., those between kin or strong bonds) that promote health. In contrast, the function of uniplex grooming relationships may be more transactional (e.g., based on social tolerance or social status) and may incur physiological costs. This complexity is important to consider for understanding the mechanisms underlying the association of social relationships on human and animal health.

FK506-binding protein 51 (FKBP51 or FKBP5) serves as a crucial stress modulator implicated in mental disorders, presenting a potential target for intervention. Inhibitors like SAFit2, rapamycin, and tacrolimus exhibit promising interactions with this protein. Despite these advances, challenges persist in diversifying FKBP5 ligands, prompting further exploration of interaction partners. Hence, this study aims to identify other potential ligands. Employing molecular docking, we generated complexes with various ligands (rapamycin, tacrolimus, SAFit2-Selective antagonist of FKBP51 by induced fit, ascomycin, pimecrolimus, rosavin, salidroside, curcumin, apigenin, uvaricin, ruscogenin, neoruscogenin, pumicalagin, castalagin, and grandinin). We identified the top 3 best ligands, of which ruscogenin and neoruscogenin had notable abilities to cross the blood-brain barrier and have high gastrointestinal absorption, like curcumin. Toxicity predictions show ruscogenin and neoruscogenin to be the least toxic based on oral toxicity classification (Class VI). Tyrosine (Tyr113) formed consistent interactions with all ligands in the complex, reinforcing their potential and involvement in stress modulation. Molecular dynamic (MD) simulation validated strong interactions between our three key ligands and FKBP5 protein and provided an understanding of the stability of the complex. The binding free energy (ΔG) of the best ligands (based on pharmacological properties) from MD simulation analysis is -31.78 kcal/mol for neoruscogenin, -30.41 kcal/mol for ruscogenin, and -27.6 kcal/mol for curcumin. These molecules, therefore, can serve as therapeutic molecules or biomarkers for research in stress-impacted mental disorders. While offering therapeutic implications for mental disorders by attenuating stress impact, it is crucial to emphasize that these ligands' transition to clinical applications necessitates extensive experimental research, including clinical trials, to unravel the intricate molecular and neural pathways involved in these interactions.

The association between the stress hyperglycemia ratio (SHR) and short-term prognosis of acute heart failure (AHF), particularly among those admitted to the intensive care unit (ICU), has not been elucidated. This study aimed to investigate the association between the SHR and adverse outcomes among critically ill patients with AHF and provide a reference for glycemic management range in these patients.

We extracted the clinical data of patients from the MIMIC-IV (v3.0) database. The association between the SHR and short-term prognosis was analyzed using the Kaplan‒Meier survival curve, Cox regression, and subgroup analysis. Important features were identified utilizing machine learning methods. Furthermore, the association between the dynamic SHR level and mortality was explored using restricted cubic splines and Cox regression.

A total of 994 patients were included. Patients with the highest SHR (Quartile 4) had a higher risk of 30-day mortality (HR = 2.14; 95% CI = 1.32-3.45; P = 0.002) and in-hospital mortality (HR = 2.22; 95% CI = 1.27-3.88; P = 0.005) than those in Quartile 2 (as reference). The results of machine learning methods revealed the SHR was an important predictor for 30-day mortality of patients with critical AHF. Restricted cubic splines indicated a J-shaped association between the dynamic SHR level and mortality, and the cut-off values were 0.84 and 1.07.

The SHR was significantly associated with 30-day mortality and in-hospital mortality among patients with critical AHF. The SHR may be a useful indicator for the glycemic management of patients with AHF in the ICU.

Extreme climatic events, like droughts, are increasing in frequency and severity. Droughts disrupt community livelihoods and resources with serious implications for human biology. This study investigated how chronic stress, measured by fingernail cortisol concentration (FCC), and water insecurity status were predictive of C-reactive protein (CRP), a biomarker of inflammation, during a historic drought among Daasanach seminomadic pastoralists.

Data were collected at the height of the 2022 drought from 128 Daasanach household heads aged 16-80 years in northern Kenya using household surveys, anthropometric measurements, and dried blood spots to assess CRP levels and fingernails to assess FCC. We employed mixed-effects linear and logistic regression models to examine the relationships between log-transformed FCC, high water insecurity status measured via the Household Water Insecurity Experiences (HWISE ≥ 24) scale, and serum-equivalent CRP (log-transformed and dichotomized at mild, low-grade inflammation ≥ 1 mg/L) adjusted for covariates.

The mean serum-equivalent CRP was 4.1 mg/L and 56.3% of Daasanach adults had at least mild, low-grade inflammation. Linear models indicated that ln(FCC) was positively associated with ln(CRP) (β = 0.56, SE = 0.12; p < 0.001). Further, logistic models demonstrated that ln(FCC) (OR = 2.69, 95% CI: 1.84-3.95; p < 0.001) and high water insecurity (OR = 2.23, 95% CI: 1.34-3.72; p = 0.002) were both associated with greater odds of low-grade inflammation.

This study provides evidence for how chronic stress and severe water insecurity may impact inflammation levels among pastoralists during drought. Since inflammation is central to cardiometabolic disease etiology, this is an additional reason to mitigate the negative health impacts of droughts and water insecurity exacerbated by climate change.

Pancreatic β-cells are specialized in secreting insulin in response to circulating nutrients, mainly glucose. Diabetes is one of the most prevalent endocrine-metabolic diseases characterized by an imbalance in glucose homeostasis, which result mainly from lack of insulin production (type 1 diabetes) or insufficient insulin and peripheral insulin resistance (type 2 diabetes), both influenced by genetic and environmental components. Pancreatic β-cell dysfunction and islet inflammation are common characteristics of both types of the disease. Pancreatic islets are a highly innervated tissue whose function can be influenced by the brain, either directly through the autonomic nervous system or indirectly via neuroendocrine mechanisms. In addition, it is well-established that there is a fine-tuned communication between the immune and neuroendocrine tissues in maintaining endocrine pancreas homeostasis. Various psycho-social, physico-chemical and lifestyle environmental factors have been associated with diabetes risk. In this review, I briefly comment on certain aspects of the psycho-neuro-immune interactions that link environmental factors and the endocrine pancreas, leading to metabolic health or diabetes. Interdisciplinary research, embracing new and broader perspectives, should be conducted to explore strategies for preventing or slowing down the constant increase in diabetes worldwide.

Breast cancer is one of the most common malignancies among women, and its development involves a variety of complex molecular mechanisms. Extracellular signal-regulated kinase (ERK) and Chromogranin B (CHGB) are known to play key roles in various cancers. This study aims to explore the impact of the ERK/CHGB pathway in a chronic stress environment simulated by salbutamol on the development of breast cancer.

This study utilized female BALB/c mice to establish a breast cancer model, dividing them into control, salbutamol-treated, and salbutamol-inhibitor-treated groups. Cell culture, immunohistochemistry, Western Blot, real-time fluorescent quantitative PCR, and Transwell migration assays were employed to assess the effects of salbutamol and the ERK/CHGB pathway.

Salbutamol treatment significantly enhanced the proliferation, migration, and invasiveness of breast cancer cells, associated with the activation of the ERK pathway and the inhibition of CHGB. The salbutamol-inhibitor-treated group exhibited a marked suppression of these effects. Additionally, the interaction of the ERK/CHGB pathway in an extracellular stress environment provided advantages for the survival and proliferation of breast cancer cells.

This study demonstrates that a chronic stress environment simulated by salbutamol can promote malignant behaviors in breast cancer cells through the ERK/CHGB pathway. These findings offer new molecular targets for breast cancer treatment and highlight the potential importance of managing chronic stress and blocking specific molecular pathways in cancer therapy.

Sex differences in the neurobiology of responses to chronic stress have been widely discussed but remain poorly understood. We found that chronic unpredictable mild stress (CUMS) experienced during adolescence induced different behavioral patterns in adult males and females. Immunohistochemical analysis of the CA1 field of the dorsal and ventral hippocampus revealed no quantitative or morphological changes in astrocytes in the long term after CUMS. Real-time PCR analysis showed no increase in the expression level of SigmaR1 after CUMS relative to individual housekeeping genes. Analysis of mouse cerebral cortex homogenates showed that IL-1β levels only decreased after CUMS in males. However, the SigmaR1 levels were significantly higher in the CUMS groups than in the control groups in both sexes. It can be concluded that biological sex and age influence the response to CUMS, although not in all cases. Further studies are needed to understand the effects of chronic stress on males and females. This is important because men and women have different risks for stress and mental disorders.

To assess whether infertile women's psychological conditions, such as depression, anxiety, and stress, are associated with in vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) outcomes, we systematically searched for relevant articles from January 1, 2004, to March 29, 2024, in five databases, including PubMed, Web of Science, EMBASE, Cochrane Library, and PsycINFO. A random-effects model was used to examine pooled standardized mean differences (SMD) and 95% confidence interval (CI). A total of 29 articles fulfilled the inclusion criteria and were included in this meta-analysis. The statistical analysis revealed that infertile women with higher levels of anxiety [SMD: -0.17, 95% CI: (-0.27, -0.06), P = 0.002] and depression [SMD: -0.17, 95% CI: (-0.30, -0.04), P = 0.008] were less likely to have a successful pregnancy following IVF/ICSI treatment. Although not statistically significant, the results indicate a trend of increasing IVF/ICSI success with increasing participants' perceived stress levels [SMD: 0.09, 95% CI: (-0.01, 0.19), P = 0.07]. There was also no statistically significant correlation between infertility-related stress and IVF/ICSI outcomes [SMD: -0.26, 95% CI: (-0.79, 0.28), P = 0.35]. In general, it suggested that medical personnel should be aware of the mental health of infertile women involved in IVF/ICSI.

In today's fast-paced society, stress has become a widespread phenomenon, garnering increasing attention for its impact on cancer. This study aims to investigate the current status and research hotspots of chronic stress in cancer research from 2014 to 2024, with the goal of providing valuable insights for future studies.

We retrieved 618 articles published between 2014 and 2024 from the Web of Science database and analyzed them using R software, VOSviewer, and CiteSpace.

There is an overall upward trend in chronic stress-related cancer research, with China leading in publications, followed by the United States, India, Australia, and Italy. The journal most cited is Brain Behavior and Immunity. Key themes identified include 'inflammation', 'breast cancer', 'anxiety', 'psychological stress', and 'oxidative stress'. The primary focus of the research is the impact of chronic stress on various cancer types, the underlying molecular mechanisms, and the implications of chronic stress-related treatments on cancer outcomes.

Chronic stress is increasingly recognized as a Carcinogenic factors. This study provides a comprehensive analysis of chronic stress-related cancer research from 2014 to 2024, offering valuable guidance for future research in this field.

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.

Repetitive stress is at the nexus of acute and chronic stress, and there is limited knowledge about how physiological and emotional responses change with repeated exposure.

We examined stress-related biomarkers and emotional responses to repeated social stressors, and we tested behavioral moderators.

In Study 1, 42 adults completed the Trier Social Stress Test (TSST) twice, 4 months apart. Serum inflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor-α [TNF-α]), blood pressure, pulse, salivary cortisol, and state-level anxiety were measured surrounding the stressor. In Study 2, 84 married individuals completed two 20-minute discussions of contentious topics in the marriage, 1 month apart. Serum IL-6, TNF-α, blood pressure, pulse, salivary cortisol, and state affect were collected surrounding the conflict. Trained experimenters rated positive and negative behavior during the conflict.

In the repetitive Trier paradigm, participants reported less anxiety (Ps = .048) and had higher anticipatory IL-6 responses (P = .014) at Visit 2, compared to Visit 1. In the repetitive marital conflict paradigm, participants had lower positive affect (P = .0004), as well as systolic blood pressure (SBP) (P = .009), diastolic blood pressure (P = .0003), and pulse (P = .027) habituation at the second visit. Objectively rated negative conflict behavior interacted with visit to predict TNF-α (P = .025) and SBP (P = .037) responses. Positive conflict behavior did not moderate outcomes (Ps > .06).

Stress-sensitive systems can habituate or sensitize to even nontraumatic, repetitive social stressors. Patterns of habituation or sensitization may vary by time between repetition, type of social stressor, stress-sensitive system, and participant behavior.

Objectives: To systematically synthesize the current evidence on the effects of art-based interventions on improving anxiety, depression, stress, sleep, and well-being of cancer caregivers. Design: A systematic review. Methods: We searched PubMed, EMBASE, Web of Science, CINAHL, PsycINFO, and Cochrane Central Register of Controlled Trials databases from their inception up to April 2024. Studies exploring the effects of art-based interventions on the psychological symptoms of cancer caregivers were included. We did not restrict the publication to the particular study designs, including randomized controlled trials, quasiexperimental studies, and qualitative studies. Results: Fifteen studies of 607 participants were identified in this systematic review. Overall, the existing studies provided preliminary evidence to suggest that art-based interventions may benefit cancer caregivers in improving anxiety, depression, stress, caregiver burden, and quality of life. However, the relatively low quality of the current evidence limits the efficacy of these findings. Conclusions: According to the existing evidence, the therapeutic benefits of using art-based interventions for improving the psychological well-being of cancer caregivers are uncertain. More high-quality and well-designed studies are still required to confirm the psychological effectiveness of art-based interventions for cancer caregivers in the future.

Fatigue is a common and debilitating symptom of a broad spectrum of diseases. Previous research has shown that individuals suffering from chronic forms of fatigue experience significantly more stress compared to healthy individuals, suggesting that stress is a potential pathophysiological factor in the onset and maintenance of chronic fatigue. Individually, chronic experiences of fatigue and stress have been associated with disruptions in adaptive immunity. However, how chronic fatigue and chronic stress together affect immune regulation is not fully understood. Here, we investigated the unique and combined contribution of chronic fatigue and chronic stress on immune cell redistribution in response to, and recovery from, acute psychosocial stress. Eighty women with high or low levels of chronic fatigue and varying levels of chronic stress were exposed to a psychosocial laboratory stressor. Blood samples were collected 10 min before and then at 10, 40, and 100 min after the end of stress. The main lymphocyte subpopulations (CD3+, CD3 + CD4+, CD3 + CD8+, CD16 + CD56+, and CD19 + cells) were enumerated via flow cytometry. Acute stress resulted in an increase in CD8 + and CD16+/CD56 + cells, a decline in CD4 + cells, and no effects on CD19 + B lymphocytes. Importantly, the magnitude of immune cell redistribution during stress reactivity (CD3+, CD4+, CD16+/CD56 + ) and recovery (CD3 + ) was contingent on fatigue and chronic stress levels of individuals. Notably, in contrast to low-fatigued individuals, who showed steeper changes in cell populations, increasing levels of chronic stress did not impact immune cell migration responses in high-fatigued individuals. Our findings demonstrate the compounded blunting effects of fatigue and chronic stress on adaptive immune functioning, highlighting a potential pathway for vulnerability and detrimental effects on long-term health.

In a subset of patients with mental disorders, such as depression, low-grade inflammation and altered immune marker concentrations are observed. However, these immune alterations are often assessed by only one data type and small marker panels. Here, we used a transdiagnostic approach and combined data from two cohorts to define subgroups of depression symptoms across the diagnostic spectrum through a large-scale multi-omics clustering approach in 237 individuals. The method incorporated age, body mass index (BMI), 43 plasma immune markers and RNA-seq data from peripheral mononuclear blood cells (PBMCs). Our initial clustering revealed four clusters, including two immune-related depression symptom clusters characterized by elevated BMI, higher depression severity and elevated levels of immune markers such as interleukin-1 receptor antagonist (IL-1RA), C-reactive protein (CRP) and C-C motif chemokine 2 (CCL2 or MCP-1). In contrast, the RNA-seq data mostly differentiated a cluster with low depression severity, enriched in brain related gene sets. This cluster was also distinguished by electrocardiography data, while structural imaging data revealed differences in ventricle volumes across the clusters. Incorporating predicted cell type proportions into the clustering resulted in three clusters, with one showing elevated immune marker concentrations. The cell type proportion and genes related to cell types were most pronounced in an intermediate depression symptoms cluster, suggesting that RNA-seq and immune markers measure different aspects of immune dysregulation. Lastly, we found a dysregulation of the SERPINF1/VEGF-A pathway that was specific to dendritic cells by integrating immune marker and RNA-seq data. This shows the advantages of combining different data modalities and highlights possible markers for further stratification research of depression symptoms.

Does the practice of yoga impact stress? Various studies have suggested that yoga may reduce both self-reported stress and stress biomarkers, but the evidence for such claims remains inconclusive, especially for yoga styles with a focus on physical postures. In a randomized controlled trial with 98 participants, we therefore examined whether an eight-week Hatha yoga intervention (60 min, 3×/week or more) led to reduced levels of diurnal salivary cortisol (sCort), salivary alpha-amylase (sAA), and subjective momentary stress as compared to a waitlist control group. To ensure the concomitant assessment of self-report and biological measures in an ecologically valid setting, and to capture the diurnal profile of cortisol and alpha-amylase, we employed an ecological momentary assessment approach. Five times per day, participants reported their momentary stress levels on a visual analogue scale and collected saliva samples for the assessment of salivary biomarkers. The intervention led to a significant reduction of subjective momentary stress but there was no change in diurnal sCort or sAA levels. There are several potential explanations for these findings: The intervention may have helped participants to cope better with stress while leaving diurnal levels of stress biomarkers unaffected, or the change may at least not have been reflected in sCort and sAA. Alternatively, there may have been a self-report bias, insofar as a favorable disposition towards yoga may have led participants to report reductions in stress in order to indicate positive effects of the intervention. Our findings contribute to a better understanding of the effects of distinct yoga interventions, demonstrating their potential to serve as low-risk stress relief tools.

Mood disorders include a set of psychiatric manifestations of increasing prevalence in our society, being mainly represented by major depressive disorder (MDD) and bipolar disorder (BD). The etiopathogenesis of mood disorders is extremely complex, with a wide spectrum of biological, psychological, and sociocultural factors being responsible for their appearance and development. In this sense, immune system dysfunction represents a key mechanism in the onset and pathophysiology of mood disorders, worsening mainly the central nervous system (neuroinflammation) and the periphery of the body (systemic inflammation). However, these alterations cannot be understood separately, but as part of a complex picture in which different factors and systems interact with each other. Psychoneuroimmunoendocrinology (PNIE) is the area responsible for studying the relationship between these elements and the impact of mind-body integration, placing the immune system as part of a whole. Thus, the dysfunction of the immune system is capable of influencing and activating different mechanisms that promote disruption of the psyche, damage to the nervous system, alterations to the endocrine and metabolic systems, and disruption of the microbiota and intestinal ecosystem, as well as of other organs and, in turn, all these mechanisms are responsible for inducing and enhancing the immune dysfunction. Similarly, the clinical approach to these patients is usually multidisciplinary, and the therapeutic arsenal includes different pharmacological (for example, antidepressants, antipsychotics, and lithium) and non-pharmacological (i.e., psychotherapy, lifestyle, and electroconvulsive therapy) treatments. These interventions also modulate the immune system and other elements of the PNIE in these patients, which may be interesting to understand the therapeutic success or failure of these approaches. In this sense, this review aims to delve into the relationship between immune dysfunction and mood disorders and their integration in the complex context of PNIE. Likewise, an attempt will be made to explore the effects on the immune system of different strategies available in the clinical approach to these patients, in order to identify the mechanisms described and their possible uses as biomarkers.

The acute stress response affects brain metabolites closely linked to the tricarboxylic acid (TCA) cycle. This response involves time-dependent changes in hormones and neurotransmitters, which contribute to resilience and the ability to adapt to acute stress while maintaining homeostasis. This physiological mechanism of metabolic dynamics, combined with time-series analysis, has prompted the development of new methods to observe the relationship between TCA cycle-related brain metabolites. This study aimed to observe the acute stress response through metabolic interactions using time-series proton magnetic resonance spectroscopy (1H-MRS) in the left hippocampus of mice.

In this study, 4-week-old male C57BL/6N mice (n = 24) were divided into control (n = 12) and acute stress groups (n = 12). Acute stress was induced through a 2 h restraint protocol. Time-series 1H-MRS data were obtained on the left hippocampus of both groups using a 9.4 T 1H-MRS scanner. Time-series MRS data were quantified using LCModel, and significant metabolic interactions were identified through Spearman correlation analysis, a one-tailed sign test, and false discovery rate correction.

No significant metabolic correlation coefficient was observed in the control group. However, in the acute stress group, glutathione (GSH) and N-acetyl aspartate (NAA) showed a significant positive correlation over time, with a high correlation coefficient exceeding 0.5.

Temporal measurement of GSH and NAA, combined with correlation analysis, offers a comprehensive understanding for the metabolic dynamics during acute stress. This approach emphasizes their distinct roles and interdependence in the progression of oxidative stress, mitochondrial function, and the maintenance of physiological homeostasis.

Stress is ubiquitous in our modern society and contributes to many disease states. This narrative review describes the effect of stress/distress on cancer development and progression. Seminal randomized controlled trials, systematic reviews/meta-analyses, and distress management guidelines from the National Comprehensive Cancer Network (NCCN), the American Society of Clinical Oncology (ASCO), and the Society for Integrative LinearOncology (SIO) are highlighted. We describe the physiological effects of distress, distress assessment, and management. Psychological treatments are summarized. Evidence-based lifestyle modifications and integrative therapies are reviewed in detail, including mindfulness-based techniques, yoga, guided imagery, breathing techniques, hypnosis, exercise, music therapy, qigong/Tai Chi, eye movement desensitization and reprocessing, and improving sleep and heart rate variability. Recognition and treatment of distress can improve quality of life. More research is needed to determine the effects of managing distress on cancer outcomes, as well as the best type and duration of intervention, noting that the benefits of interventions may be specific for patients with different cancer types.

Chronic low back pain (cLBP) is a complex disease with biological, psychological, and social components and the complex interactions of these components are poorly understood. Chronic psychological stress (CPS) (anxiety, depression, etc.) and pathological changes in spinal tissue (osteoporosis, disc degeneration, etc.) are frequently and independently associated with cLBP, yet their explicit relationship has not been collectively reviewed. The objective of this scoping review is to investigate the current state of research on how CPS may impact spinal tissue pathology.

Five steps were utilized to conduct this scoping review: 1) identify a research objective and establish a search strategy, 2) identify research articles, 3) select research articles that meet search criteria, 4) extract data, 5) summarize and report results.

We identified N ​= ​56 articles relating CPS to spinal pathology. Of those that identified a relationship between CPS and spine pathology (N ​= ​39), most (N ​= ​24) described decreased lumbar vertebral bone mineral density (BMD) between depression and control groups. Animal studies (N ​= ​8) were limited to mice and confirmed a causal relationship between CPS and lower vertebral BMD. Only a few additional human studies (N ​= ​9) documented relationships between other various forms of CPS and spinal tissue pathologies.

This scoping review documents evidence of a relationship between CPS and decreased spine health in humans as well as a causal relationship between the initiation of CPS and decreased BMD in animals. As few studies evaluated disease in other spinal anatomy in relationship to CPS, future work in this area is warranted. Further exploration of CPS beyond depression is warranted as well.

Functional cognition is relevant for athletic success and interdependent with physical exercise, yet despite repeatedly demonstrated inflammatory responses to physical training, there are no studies addressing the relationship between cognition and inflammation in athletes. The aim of this study was to investigate the relationship between cognitive performance and selected inflammatory, and further physiological biomarkers in elite athletes. Data from 350 elite athletes regarding cognitive performance (processing speed, selective attention, working memory, cognitive flexibility), systemic inflammatory markers, metabolic hormones, growth factors, tissue damage markers, and micronutrients (e.g., ferritin, 25-OH-vitamin D), as well as physiological, subjective ratings of recovery and stress were analysed by correlative and multiple regression analyses. Results show that across all athletes variance in processing speed, selective attention, and working memory, could be best explained through a combination of metabolic hormones with physiological and psychological indicators of stress, and in cognitive flexibility through vitamin D levels. Only for the subgroup of athletes from closed-skill sports, the ratio TNF-α:IL-10 significantly contributed to explanation of variance in working memory and cognitive flexibility. In general, found correlations point to the importance of inflammatory balance and sufficient long-term nutrient supply for unaffected cognitive performance.

We examined the feasibility of using the neofunctional deep breathing (NDB) technique to reduce the allostatic load following the Trier Social Stress Test (TSST). Forty-four healthy subjects were randomised into experimental and control groups. Following the TSST procedure, participants underwent either a single session of NDB or an attention control intervention. The Procomp Infinity Biofeedback system measured breath per minute (BPM), respiratory amplitude, HRV linear domains, skin conductance, and trapezius muscle electromyographic activity. Cortisol and cytokine salivary concentrations, perceived stress, and anxiety levels were also assessed. These parameters were combined into an allostatic load index (ALI) to measure the intervention's effect. This pilot RCT demonstrated the feasibility of the study design and practicality of the intervention. The NDB group showed reduced ALI, increased respiratory abdominal amplitude, decreased BPM, increased HRV indicating parasympathetic activation, and decreased cortisol and inflammatory cytokines. This study highlighted the feasibility of testing the NDB technique in reducing allostatic load through a neurobiological and anti-inflammatory response after exposure to psychosocial stress. This protocol can represent a non-invasive therapeutic adjutant in disorders related to a dysregulation of the HPA axis or to an inflammatory state. Trial Registration: NCT04102813.

To date, few studies have considered the influence of psychological factors on chronic prostatitis (PRO) models. Here, we aimed to refine a murine PRO model combining chemically induced prostatitis with psychological stress.

A total of 40 mice were randomly divided into four groups: normal control (NC) group, PRO group, water avoidance stress (WAS) group, and PRO + WAS group. Ten mice were assigned to each group: five for cystometrograms (CMGs) and five for von Frey testing and histological analysis. PRO was induced through a prostatic injection of 10% paraformaldehyde. The WAS mice were placed on the middle platform for 1 h per day for 10 consecutive days.

The results of the von Frey test demonstrated that both WAS and PRO induced bladder hyperalgesia in mice, and the WAS + PRO group showed significant pelvic pain symptoms either. The CMG results suggested that the PRO group, the WAS group, and the PRO + WAS group all exhibited bladder overactivity, presented as a shortened micturition interval and decreased threshold pressure evoking bladder contraction. The symptoms of the PRO group and the PRO + WAS group were more severe than those of the WAS group. The tissue staining results indicated that WAS itself caused only mild prostatic inflammation but could significantly aggravate chemical-induced prostatic inflammation, as well as the total number of mast cells and proportion of activated mast cells.

Our refined murine PRO model could manifest persistent bladder overactivity, pelvic hyperalgesia and prostatic inflammation. WAS could induce mild prostatic inflammation and aggravate primary prostatic inflammation.

The vertebrate stress response enables an organism to shift energy towards activities that promote immediate survival when facing a threat to homeostasis, but it can also have detrimental effects on organismal health. Acute and chronic stressors generally have contrasting effects on immune responses, but the timeline of this transition between acute and chronic stressors and their effects on immune responses remains unclear. In this study, we investigate changes in immune markers in captive house sparrows (Passer domesticus) after exposure to normal laboratory conditions, an acute stressor, and chronic stressors for 42 days. Specifically, we examined changes in baseline and stress-induced corticosterone concentrations, body condition, heterophil/lymphocyte (H:L) ratio, hemolysis-hemagglutination, and wound healing. We found that individuals exposed to a single acute stressor had significantly higher stress-induced corticosterone concentrations 24 h after stressor exposure, however this effect was reversed after 48 h. Chronic stressor exposure resulted in generally stronger adaptive immune responses, demonstrated by higher baseline and stress-induced lysis, higher baseline hemagglutination, and slower wound healing. Within-trait correlations also increased with chronic stressor exposure, suggesting limitations on phenotypic plasticity. Most of the effects of chronic stressor exposure on immune markers strengthened over the 42 days of the experiment and differences between captivity-only and treatment groups were not apparent until approximately 20 days of chronic stressor exposure. These results highlight the importance of stressor duration in understanding the effects of chronic stressor exposure on immune responses.

Cognitive behavioral therapy for insomnia (CBT-I) is a widely used psychological intervention known for its effectiveness in improving insomnia symptoms. However, the neurophysiological mechanisms underlying the cognitive-behavioral treatment of insomnia remain unclear. This narrative review aimed to elucidate the neurophysiological and molecular mechanisms of CBT-I, focusing on the fields of psychology, neurophysiology, neuroendocrinology, immunology, medical microbiology, epigenetics, neuroimaging and brain function. A comprehensive search was conducted using databases including: PubMed, Embase, PsycINFO and Web of Science, with customized search strategies tailored to each database that included controlled vocabulary and alternative synonyms. It revealed that CBT-I may have a beneficial effect on the central nervous system, boost the immune system, upregulate genes involved in interferon and antibody responses, enhance functional connectivity between the hippocampus and frontoparietal areas and increase cortical gray matter thickness. In conclusion, an integrated model is proposed that elucidates the mechanisms of CBT-I and offers a new direction for investigations into its neurophysiological mechanisms.

Background: Metabolic inflammation (MI), long COVID (LC) and systemic lupus erythematosus (SLE) share some metabolic common manifestations and inflammatory pathophysiological similarities. Health-related quality of life (HRQoL) and metabolic age are indicators of health status. The "METAINFLAMMATION-CM Y2020/BIO-6600" project, a prospective controlled study, aimed to identify differential diagnostic tools and clinical features among three inflammatory conditions by comparing obesity status (low BMI vs. high BMI). Methods: A total of 272 adults of both Caucasian and Hispanic descent, diagnosed with MI, LC or SLE, and a range of BMI, were recruited. Clinical and phenotypic traits were measured to analyze body composition, metabolic and inflammatory markers, HRQoL data, metabolic age and lifestyle habits using a 3 × 2 (disease × BMI) factorial design. Results: Some inflammatory related variables, such as fibrinogen, RDW (red cell blood distribution width), ESR (erythrocyte sedimentation rate) and NLR (neutrophil/lymphocyte ratio), showed effect modifications depending on the BMI and disease type. In relation to HRQoL, the Physical Component Summary (PCS12) showed no relevant changes, while the Mental Component Summary (MCS12) showed a significant effect modification according to the disease type and BMI (p < 0.05). Furthermore, a significant interaction was identified between the disease type and BMI in relation to metabolic age (p = 0.02). Conclusions: Assessing the impact of BMI on these three inflammatory diseases may help to prevent clinical complications and to design personalized treatments, especially for patients with SLE, who have a worse prognosis with an increased BMI compared to the other two inflammatory diseases.

Research about the impact of acute stress on inhibitory control remains a contentious topic, with no consensus reached thus far. This study aims to investigate the effects of acute stress on an individual's inhibitory control abilities and to elucidate the underlying neural mechanisms by analyzing resting state electroencephalogram (EEG) data.

We recruited 32 male college students through participant recruitment information to undergo within-subject experiments under stress and non-stress conditions. Physiological indicators (cortisol and heart rate), self-report questionnaires, and behavioral data from the Stroop task were collected before, during, and after the experiment. Additionally, a five-minute eyes closed resting state EEG data collection was conducted during the Stroop task before.

(1) Acute stress led to a reduction in the conflict effect during the participants' Stroop task in individuals. (2) Stress resulted in an increase in the power of the beta in the resting state EEG. (3) Acute stress caused an increase in the duration of class D and an increase in the transition probabilities from classes C and B to class D in the microstates of the resting state EEG. (4) Acute stress leads to an increase in beta power values in individuals' resting state EEGs, which is significantly negatively correlated with the reduction of the conflict effect in the Stroop task under stress.

Acute stress can enhance individuals' attentional level, thereby promoting inhibitory control performance.

Gestational metabolic diseases adversely impact the health of pregnant persons and their offspring. Pregnant persons of color are impacted disproportionately by gestational metabolic disease, highlighting the need to identify additional risk factors contributing to racial-ethnic pregnancy-related health disparities. Trauma exposure and posttraumatic stress disorder (PTSD) are associated with increased risk for cardiometabolic disorders in nonpregnant persons, making them important factors to consider when identifying contributors to gestational metabolic morbidity and mortality health disparities. Here, we review current literature investigating trauma exposure and posttraumatic stress disorder as psychosocial risk factors for gestational metabolic disorders, inclusive of gestational diabetes, low birth weight and fetal growth restriction, gestational hypertension, and preeclampsia. We also discuss the physiological mechanisms by which trauma and PTSD may contribute to gestational metabolic disorders. Ultimately, understanding the biological underpinnings of how trauma and PTSD, which disproportionately impact people of color, influence risk for gestational metabolic dysfunction is critical to developing therapeutic interventions that reduce complications arising from gestational metabolic disease. KEY POINTS: · Gestational metabolic diseases disproportionately impact the health of pregnant persons of color.. · Trauma and PTSD are associated with increased risk for cardiometabolic disorders in nonpregnant per.. · Trauma and PTSD impact physiological cardiometabolic mechanisms implicated in gestational metabolic..

Hair cortisol concentration (HCC) indicates chronic stress exposure, which is a risk factor in the pathogenesis of burnout and depression. However, findings on HCC are inconsistent. Similarly, intervention studies show mixed effects on HCC. The present study aimed to shed light on these inconsistencies, by additionally considering also hair cortisone.

Twenty-five patients with a burnout-related depressive disorder receiving a multimodal inpatient treatment for clinical burnout and 17 matched healthy controls participated in this study. All participants provided 1 cm long hair samples at the beginning and end of the treatment. HCC and hair cortisone levels (HCNC) were determined. Meteorological data and duration of sick leave were considered as potential covariates. Burnout and depression were assessed with self-ratings, the latter also with examiner ratings.

There were no significant group differences in glucocorticoid levels. Treatment led to a decrease in both depression severity and hair glucocorticoid concentration in inpatients, while lower HCNC in particular predicted a greater reduction in depression severity. Moreover, meteorological data and the duration of sick leave were also found to have an effect on hair glucocorticoid concentrations.

These results suggest that multimodal inpatient treatment of clinical burnout considerably reduced stress on both a psychological and biological level. In parallel, hair glucocorticoids appear to be sensitive biomarkers for the evaluation of treatment success and prediction. Examining both HCC and HCNC in intervention studies may provide clearer results than the usual examination of HCC alone.

Higher levels of social capital (SC) are associated with better health status. However, there is little evidence of the impact of SC on biological health outcomes in the early ages. To identify the association between SC in adolescence and inflammation levels in early adulthood. Prospective study using data from 2435 participants from the Epidemiological Health Investigation of Teenagers in Porto cohort. SC was assessed at age 17 through a self-administered questionnaire, and high-sensitivity C-reactive protein (hs-CRP) and leucocytes were measured in a fasting blood sample at 17 and 21 years-old. A principal components analysis was performed to identify the domains of SC. Simple linear regressions were performed to assess the association between SC components and inflammatory status at 17 and 21 years old. Pathway analysis was performed to assess the direct, indirect, and total effects of SC on hs-CRP and leucocyte levels. We did not find a significant total effect between SC at 17 years-old and hs-CRP at 21 years-old. However, the Trust/Reciprocity dimension showed a significant direct effect between SC and hs-CRP levels at 21 (β = -0.065, 95% CI: -0.129; -0.001), as well as a significant total effect (β = -0.075, 95% CI: -0.139; -0.011). Regarding leucocyte levels, total SC at 17 years-old was associated with leucocytes levels at 21 (β = -0.115, 95% CI: -0.205; -0.024). Significant direct (β = -0.104, 95% CI: -0.194; -0.014) and total effect (β = -0.107, 95% CI: -0.199; -0.015) of Trust/Reciprocity on leucocyte levels were observed. Adolescents with higher SC have a low inflammatory level in early adulthood, especially those with greater levels of trust/reciprocity.

The positive impact of essential oils (EOs) on stress release has been demonstrated in both humans and dogs. Among the EOs known for their anxiety-reducing properties, including Cananga odorata, Citrus aurantium, Cupressus sempervirens, Lavandula angustifolia, and Litsea citrata, there is a lack of consensus on the optimal concentration for efficacy. This exploratory study sought to investigate the effects of olfactory enrichment with a blend of these EOs on dogs introduced to an unfamiliar environment. The authors sought to determine the minimum concentration required to achieve increased relaxation. In a randomized controlled crossover study design, 54 dogs were exposed to 0, 1, 5, and 10 drops of the EO blend applied to their collars before entering an unfamiliar room with their owners. Behavioral observations were employed to quantify the total duration of activity and relaxation related behaviours for each dog under each treatment condition. A significant difference in panting was identified among the treatments (χ2(3) = 9.88; p = 0.020). Dunn-Bonferroni post-hoc tests revealed a significant reduction in panting during the 10 drops treatment compared to the control treatment (p = 0.047). No significant differences were observed for other behaviors. To provide a comprehensive overview of behavioral tendencies in this canine population, owners also completed the Canine Behavioral Assessment and Research Questionnaire (C-BARQ), revealing low scores for anxiety in the study group. These preliminary findings suggest that a concentration of 10 drops of the EO blend on a dog's collar induces increased relaxation, specifically reflected in decreased panting behavior. Lower concentrations did not exhibit a significant relationship with the observed behaviors. These initial findings underscore the importance of exposing dogs to an appropriate concentration of EOs when exploring their potential benefits on welfare among dogs with low anxiety levels. Further research in this area is crucial for a comprehensive understanding of the potential benefits of EOs for canine welfare.

A Randomized Controlled Trial involving 158 Brazilian medical and nursing students assessed one of three conditions over an 8-week period: 1) a circuit training protocol (CTG); 2) a yoga protocol (YG); or 3) no intervention (CG). The objective was to evaluate the effectiveness of circuit training and yoga protocols in reducing perceived mental stress and examining their effects on serum cortisol levels, as well as on traditional cardiovascular risk factors (CRFs), during an academic semester. Mental stress was measured using self-reported stress questionnaires. For the CTG, comparisons of pre- vs. post-intervention data indicated a reduction in self-reported stress levels on a Brazilian scale (p < 0.001) and an international scale (p < 0.05). Regarding CRFs, there was a reduction in waist circumference (WC) (p < 0.05), systolic blood pressure (SBP) (p < 0.05), and heart rate (HR) (p < 0.001). No changes were observed in diastolic blood pressure (DBP) (p = 0.211) and serum cortisol (SC) (p = 0.423). In the YG, pre- vs. post-intervention data indicated a reduction in self-reported stress levels on the ISSL (p < 0.001), in both resistance and exhaustion stress levels on the PSS scale (p < 0.001), and in SC levels (p < 0.001), WC (p < 0.05), and SBP (p < 0.05); however, HR and DBP did not change (p = 0.168 and p = 0.07, respectively) in this group. No changes were noted in any measures in the CG. The intervention protocols demonstrated that both CTG and YG can positively impact mental or biochemical stress responses, as well as CRFs.

Immigrants are exposed to a variety of stressors, such as ethnic discrimination, and therefore experience a higher risk of developing adverse health outcomes. However, the role of potentially protective psychological factors is not well-studied. The present study addresses the question how discrimination and institutional verbal violence (IVV) are associated with chronic stress in an immigrant sample. In addition, this study highlights moderating effects of migration-specific variables (first or second migration generation and citizenship status). Participants (n = 232; 69.4 % female) completed an online-survey, which included demographics, questionnaires (Everyday Discrimination Scale, EDS; Perceived Stress Scale, PSS-4; Resilience Scale, RS-11; Self-Compassion Scale, SCS-SF) as well as a self-developed questionnaire on institutional verbal violence. Only participants living in Germany with migration background (self or one parent migrated to Germany) were included. Results showed that perceived discrimination and institutional verbal violence were highly associated with chronic stress. Further, self-compassion buffered the connection between discrimination and stress, whereas resilience was no protective factor. The inclusion of migration-specific variables showed that the second-generation sub-group experienced less discrimination-related stress and self-compassion was shown to be particularly protective within this sub-group. Citizenship status did not appear to be a moderator, but especially persons with temporary or permanent residence status, compared to German/EU-citizens, reported higher values of verbal violence and discrimination-related stress. These findings highlight the importance of considering not only psychological but also structural and societal protective and risk factors, as they may be differentially associated with immigrants' stress perceptions. Implications for future research and practical implementations are presented.

The term "affective immunology" has recently been used to denote a field focused on the interplay between affective processes (including mood states, specific emotions, and regulatory processes) and various aspects of immune function. The overarching goals of this commentary are a) to provide historical underpinnings of this field with a focus on the profound impact of the work of Janice Kiecolt-Glaser, who is further honored in this special issue, b) to review important off-shoots of her legacy work in this domain, and c) to highlight important future directions for the field. Kiecolt-Glaser's work laid much of the foundation for affective immunology, with groundbreaking research related to depression, hostility and dyadic interactions, loneliness, and other affective patterns, often in the context of holistic models, novel experimental designs, and interventions. Her former mentees (and many of their mentees) have carried on her legacy in these domains, in ways that continue to advance appreciation of how affective processes relate to immune function. There are numerous remaining questions for the field to pursue, including better understanding of the role of emotion regulation, emotional reactivity and recovery, restorative processes, affective variability, and developmental and dynamic social processes. Such work will require greater use of longitudinal and within-person approaches and/or examination of processes in daily life, as well as models that account for interactive and reciprocal processes and which integrate behavior, social context, sociocultural factors, individual differences, and other aspects of health. As more work in these domains continues, building on Kiecolt-Glaser's rich legacy, we move toward the emergence of affective immunology as an important subfield in the domain of psychoneuroimmunology, one which will offer more nuanced understanding of the role of affective processes in immune health.

General peri- and postnatal characteristics may serve as markers linking pre- or early postnatal events to later health outcomes, which in turn are associated with altered stress- and immune system activity. Our exploratory study investigated whether A) the common perinatal measures "birth weight" and "birth mode" and B) the postnatal characteristics "breastfeeding" and "vaccination status" are associated with markers of stress systems - the hypothalamic-pituitary-adrenal (HPA) axis and autonomous nervous system (ANS) - and inflammation in healthy young adults (n = 68, females: 70.6 %, mean age: 24.21 years, SD = 4.38) exposed to psychosocial challenge, the 'Trier Social Stress Test' (TSST). Salivary cortisol, alpha-amylase (sAA) and plasma interleukin-6 (IL-6) were assessed before, during and after the TSST. Participants provided information on peri- and postnatal characteristics. Linear regressions were performed to determine whether peri-/postnatal variables predict basal and stress-response-related biomarker levels. Controlling for sex and sex hormone use as relevant confounders, we found a significant association between birth weight and cortisol recovery (p = 0.032), with higher birth weight predicting higher cortisol recovery values. There were no other significant associations between predictor and outcome variables. Our results show that, in healthy young adults of mixed gender, normal-ranged birth weight is related to the cortisol response to psychosocial stress, indicating a long-term association of this perinatal marker with HPA axis function. In contrast, birth weight was not associated with markers of the ANS stress response or inflammation in adulthood. Our results further suggest that the measures birth mode, duration of breastfeeding, and vaccination status at 4 months of age do not relate to markers of the inflammatory and stress systems in adulthood.

Although many breast cancer survivors adjust to cancer treatment and survivorship, a sizable subgroup of women do not do so, resulting in psychological distress. Over time, this psychological distress can contribute to immune dysfunction and accompanying worsened physical symptoms as women navigate survivorship. Dr. Kiecolt-Glaser's work and mentorship has been integral to our understanding of breast cancer survivors' immune risks, and how behavioral factors may enhance these risks. As a postdoctoral fellow in the Stress and Health Lab, under Dr. Kiecolt-Glaser's mentorship, my research focused on understanding how distress is associated with immune functioning and physical health in breast cancer survivors. In this paper, we highlight Dr. Kiecolt-Glaser's influence on our careers as a strong female research and mentor, the work completed under her mentorship, and how the field of psychoneuroimmunology can continue to expand her research to better understand how distress in the cancer context confers long-term health risks.

Cardiovascular disease (CVD) affects millions worldwide and is the leading cause of death among non-communicable diseases. Western diets typically comprise of meat and dairy products, both of which are rich in cholesterol (Cho) and methionine (Met), two well-known compounds with atherogenic capabilities. Despite their individual effects, literature on a dietary combination of the two in the context of CVD are limited. Therefore, studies on the combined effects of Cho and Met were carried out using male Sprague Dawley rats. An additional interest was to investigate the cardioprotective potential of sitagliptin, an anti-type 2 diabetic drug. We hypothesized that feeding a dietary combination of Cho and Met would result in adverse cardiac effects and would be attenuated upon administration of sitagliptin.

Adult male Sprague-Dawley rats were fed either a control (Con), high Met (1.5%), high Cho (2.0%), or high Met (1.5%) + high Cho (2.0%) diet for 35 days. They were orally gavaged with an aqueous preparation of sitagliptin (100 mg/kg/d) or vehicle (water) from day 10 through 35. On day 36, rats were euthanized, and tissues were collected for analysis.

Histopathological evaluation revealed a reduction in myocardial striations and increased collagen deposition in hypercholesterolemia (HChol), responses that became exacerbated upon sitagliptin administration. Cardiac pro-inflammatory and pro-fibrotic responses were adversely impacted in similar fashion. The addition of Met to Cho (MC) attenuated all adverse structural and biochemical responses, with or without sitagliptin.

Adverse cardiac outcomes in HChol were enhanced by the administration of sitagliptin, and such effects were alleviated by Met. Our findings could be significant for understanding or revisiting the risk-benefit evaluation of sitagliptin in type 2 diabetics, and especially those who are known to consume atherogenic diets.

Acute Stress Disorder (ASD) is a psychiatric condition that can develop shortly after trauma exposure. Although molecular studies of ASD are only beginning, groups of metabolites have been found to be significantly altered with acute stress phenotypes in various pre-clinical and clinical studies. ASD implicated metabolites include amino acids (β-hydroxybutyrate, glutamate, 5-aminovalerate, kynurenine and aspartate), ketone bodies (β-hydroxybutyrate), lipids (cortisol, palmitoylethanomide, and N-palmitoyl taurine) and carbohydrates (glucose and mannose). Network and pathway analysis with the most prominent metabolites shows that Extracellular signal-regulated kinases and c-AMP response element binding (CREB) protein can be crucial players. After highlighting main recent findings on the role of metabolites in ASD, we will discuss potential future directions and challenges that need to be tackled. Overall, we aim to showcase that metabolomics present a promising opportunity to advance our understanding of ASD pathophysiology as well as the development of novel biomarkers and therapeutic targets.

Diet directly affects glucose metabolism, and eating behavior is influenced by various daily life stressors. This study was conducted to investigate the relationship between common psychosomatic stressors on endocrine hormones and eating behavior in patients with type 2 diabetes.

This cross-sectional study was performed in 40 patients with type 2 diabetes. Resting hormone blood sampling and four self-reported questionnaires were employed.

Patients who scored higher on the 'anger/hostility' (AH) subcategory of the profile of mood state (POMS) questionnaire had significantly higher serum cortisol (β = 0.40, P = 0.01 by least squares adjusted for age and sex). In the eating behavior questionnaire, the subcategories of 'feeling of hunger/satiation' (β = 0.49, P < 0.01) and 'eating as diversion' (β = 0.39, P = 0.03) were associated with higher serum cortisol. Resting morning cortisol levels were higher in participants who rated high on the POMS-AH and in those who reported 'irritated when hungry' and 'tend to eat when irritated or anxious'. Sleep quality showed no association with eating behavior.

Mood state is associated with eating behavior. Anger increases cortisol levels and may lead to compulsive eating. Various forms of hostility are important factors in appetite control and increased cortisol secretion, and can be an impediment to successful dietary self-management in patients with type 2 diabetes. Thus, assessment of mood state and control of negative mood are important therapeutic targets in diabetes management.