Studiendatenbank

<h4>Background</h4>Since its introduction, the definition and diagnosis of burnout remain controversial. Although the literature distinguishes between severe clinical burnout, characterized by debilitating symptoms and prolonged recovery, and milder burnout complaints in generally healthy employees, unclear diagnostic criteria hinder reliable differentiation. As clinical burnout is often framed as an outcome of chronic stress, clarifying how chronic stress is defined and measured is crucial to improve the understanding, diagnosis, and distinction of clinical burnout.<h4>Objective</h4>This scoping review synthesizes results from systematic reviews using an integrative approach. It examines how chronic stress is defined and measured, from psychosocial, biological, and biopsychosocial perspectives. Additionally, it explores the discriminative value of these measurement approaches in identifying individuals at risk of chronic stress-related disorders and in diagnosing clinical burnout.<h4>Methods</h4>A systematic search was performed on April 9th, 2024, and updated on July 8th, 2025 (PsychInfo, Embase, Medline and PubMed), following the PRISMA-ScR guidelines. The search identified 2,645 abstracts, 219 were included for full text screening, and 45 reviews were analyzed, covering over 2000 studies.<h4>Results</h4>Across reviews, definitions of chronic stress varied, referring to either internal and external stressors or to stress responses. Measurements ranged from biomarkers and p

Psychological stress is a recognised, yet mechanistically unresolved, risk factor for cardiovascular disease (CVD) partly through its association with a hypercoagulable state. Free radical-mediated oxidative stress has been proposed as a key upstream driver of this haemostatic imbalance. In this randomised cross-over study we investigated whether acute psychological stress promotes systemic radical formation and prothrombotic alterations in clot microstructure in eight healthy males. The Trier Social Stress Test was used to induce psychological stress. Antecubital venous blood was collected to measure the ascorbate free radical (A^•-, electron paramagnetic resonance spectroscopy) and clot microstructure (D_f, Fourier transform rheology), alongside standard coagulometry. Compared with the control condition (quiet sitting), psychological stress increased A^•- (P = 0.042) and D_f (P = 0.008), the latter reflecting larger, denser and more fibrin-rich networks. We also observed selective shortening of activated partial thromboplastin time (aPTT) (P = 0.018), indicating activation of the intrinsic coagulation pathway. This study provides the first in vivo evidence that acute psychological stress triggers systemic free radical formation and drives prothrombotic remodelling of clot architecture. These findings identify oxidative stress as a mechanistic link between psychological stress and CVD risk and highlight it as a compelling target for pr

Autoimmune diseases are chronic inflammatory conditions characterized by the breakdown of immune tolerance to self-antigens. While genetic and environmental factors play key roles, growing evidence highlights chronic stress as a significant contributor to immune dysregulation through its impact on the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis, primarily via cortisol secretion, serves as the major neuroendocrine mediator of stress responses, influencing both immune regulation and systemic homeostasis. This review synthesizes current literature on HPA axis physiology, the mechanisms of cortisol signaling, and the maladaptive effects of chronic stress. Emphasis is placed on clinical and experimental findings linking HPA dysfunction to immune imbalance and autoimmunity, as well as organ-specific consequences across neuroimmune, endocrine, cardiovascular, gastrointestinal, integumentary, and musculoskeletal systems. Chronic stress leads to impaired HPA axis feedback, glucocorticoid receptor resistance, and paradoxical cortisol dysregulation, fostering a pro-inflammatory state. This dysregulation promotes cytokine imbalance, weakens protective immune mechanisms, and shifts the immune response toward autoimmunity. Evidence from both human and animal studies associates persistent HPA dysfunction with diseases such as systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. HPA axis dysregulation under chronic stress constitutes a critical mechanistic

Socio-economic and environmental factors significantly influence health by driving epigenetic changes that alter genetic expression and impact disease prevention. Lifestyle elements such as diet, exercise, mindfulness, and environmental exposure play crucial roles in modulating these mechanisms. A systematic review of studies from the past 13 years, conducted under PRISMA guidelines, examined interventions, epigenetic outcomes, and health impacts. Mindfulness practices, particularly meditation, were found to regulate DNA methylation, reducing stress and inflammation. Dietary interventions, such as the Mediterranean and DASH diets, enhanced health biomarkers and slowed epigenetic aging through favorable DNA methylation. Physical activities, such as high-intensity interval training and hybrid training, induced epigenetic modifications, improving metabolic function, mitochondrial biogenesis, and insulin sensitivity. These findings emphasize the importance of adopting modern lifestyle choices to promote health and prevent chronic diseases by influencing gene expression. Combining mindfulness, balanced diets, and regular physical activity offers substantial benefits for metabolic, cardiovascular, and mental health. However, more research is needed to understand the long-term effects of lifestyle factors on epigenetics and to develop personalized strategies that optimize disease prevention and overall wellbeing.

<b>Background/Objectives</b>: The study aimed to examine the impact of allostatic load on healthy ageing over a decade and whether social participation attenuates this relationship among older American adults. <b>Methods</b>: Data were extracted from three waves (wave 8, wave 10, wave 13) of the Health and Retirement Study, a longitudinal survey of American adults. The analysis included allostatic load, socioeconomic (education) and demographic (gender, age, ethnicity, and marital status) factors at baseline, social participation in wave 10, and healthy ageing in wave 10 and wave 13. A latent variable was created for allostatic load that included waist circumference, C-reactive protein, glycated hemoglobin, and blood pressure. Healthy ageing was defined as an aggregate measure including freedom from disability, freedom from cognitive impairment, and high physical functioning. Social participation was a dichotomous variable that included individuals' work status, perceived neighbourhood safety, and partaking in volunteer work. Structural equation modelling was used to examine the direct and indirect relationships between these factors and healthy ageing. <b>Results</b>: A total of 14,537 participants with complete data in all waves were included in the analysis. The mean age at baseline was 68.7 years. Results showed a significant association between higher allostatic load and lower healthy ageing (estimate = -0.12, 95% CI: -0.14, -0.11). Allostatic load was negatively associa

<b>Background/Objectives:</b> Chronic exposure to stress has been considered a risk factor for hypertension, which is also associated with increased bone resorption. This review aimed to investigate the effect of acute and chronic stress, associated with hypertension, on the skeletal system. <b>Methods:</b> A comprehensive search was conducted across multiple databases, focusing on peer-reviewed articles published in English. We include experimental, clinical, and peer-reviewed studies focused on the relationship between stress, hypertension, and bone resorption. Searches were conducted in MEDLINE via PubMed, Embase and Scopus, with the last search completed on 10 September 2024. <b>Results:</b> The main topics include situations that favor bone loss, such as psychological stress, which can lead to osteoporotic fractures through immunological and endocrine mechanisms. The relationship between psychological stress and loss of bone density, as in osteoporosis, occurs due to the reduction in the number of osteoblasts and loss in the balance between physiological formation/resorption. <b>Conclusions:</b> Chronic stress significantly affects cardiovascular health and bone resorption. This narrative review study highlights the vulnerability of the skeletal system, along with the cardiovascular system, to prolonged stress, emphasizing the need for multidisciplinary strategies in preventing stress-related conditions. Effective stress management can help reduce the risks of cardiovasc

<h4>Background</h4>Oxidative stress and inflammation contribute to telomere length (TL) attrition, a hallmark of cellular senescence. Systemic lupus erythematosus (SLE) is associated with premature cellular aging; however, the clinical relevance of TL shortening remains unclear. This study aimed to compare the relative TL of SLE patients and healthy controls and explore its association with clinical features and disease burden.<h4>Methods</h4>We conducted a cross-sectional study including adult SLE patients and age- and sex-matched healthy controls (18-60 years). Demographic and clinical data were collected, and TL was measured using quantitative polymerase chain reaction (qPCR). Among SLE patients, disease activity, cumulative damage, fatigue, depression, anxiety, stress, and physical activity were also assessed. Statistical analyses included descriptive statistics, Student's t-test or Mann-Whitney test for group comparisons, Spearman's correlation, and multiple linear regression models selected based on the lowest Akaike information criterion (AIC).<h4>Results</h4>Sixty SLE patients (37 years ± 11.5) and 55 controls (38 years ± 10.5) were enrolled. SLE patients exhibited significantly shorter TL [median (IQR): 0.80 (0.29-2.94)] compared to controls [1.07 (0.38-2.32); p = 0.005]. In multivariate analysis, moderate anxiety was associated with shorter TL compared to none/low anxiety [β= -0.353 (95%CI: -0.645; -0.061); p = 0.019]. An alternative model indicated that moderate st

Chronic stress has been shown in cross-sectional as well as longitudinal studies to be strongly associated with diabetes, hypertension, and cardiovascular disease (CVD). These studies have used various methods of stress assessment. Proposed pathogenetic mechanisms linking psychological distress with diabetes and CVD are complex and include stimulation of the hypothalamic-pituitary-adrenal axis with excess cortisol release, as well as stimulation of the renin-angiotensin-aldosterone system, resulting in elevated blood pressure, in addition to an altered immune system, increased inflammation, and oxidative stress, among others. In this review, we provide the reader with cutting-edge information on the current evidence for the association between chronic psychological stress, diabetes, and CVD, highlighting the major studies addressing this important topic. We also provide a detailed mechanistic overview of the pathogenesis of diabetes and CVD in psychologically stressed individuals, including experimental and laboratory evidence. We finally discuss the major evidence-based therapeutic interventions for psychological stress and their effects on CVD risk reduction, with the aim of presenting these therapeutic options as potentially effective ways to implement in clinical practice.

This narrative review explores the integration of mindfulness-based interventions (MBIs) into musculoskeletal (MSK) care, based on the premise that addressing the mind-body interface can enhance patient outcomes. First, we outline how chronic stress affects twelve physiological systems and contributes to the onset and persistence of MSK conditions. Second, we synthesise evidence showing that MBIs mitigate these stress effects through mechanisms such as improved attention regulation, interoceptive awareness, and reduced catastrophising. Third, we highlight Neuro-Emotional Technique (NET) as a practitioner-facilitated hybrid-MBI exemplar that targets unresolved emotional stress patterns and aligns with the biopsychosocial model of healthcare. We also note contraindications via red and yellow flag considerations, emphasising the importance of careful patient selection and responsible application. Taken together, this review provides a rationale for incorporating MBIs as adjuncts to conventional therapies, supporting recovery, fostering resilience, and advancing patient-centred MSK care.

Chronic stress has emerged as a critical global public health threat, acting as a risk hub that mediates the onset and progression of diverse psychosomatic diseases (e.g., cardiovascular diseases, mental disorders, metabolic syndrome, and even cancer) through interconnected biological pathways. This review systematically elaborates on the core biological mechanisms underlying chronic stress-induced psychosomatic dysfunction, including hypothalamic-pituitary-adrenal (HPA) axis dysregulation, autonomic nervous system (ANS) imbalance, abnormal inflammatory responses, and excessive oxidative stress-with precise corrections to factual descriptions of neuroendocrine signaling. From a clinical nursing perspective, we critically evaluate existing evidence for each pathway, identify key gaps in current research, and strengthen the mechanistic link between targeted nursing interventions and biological pathway modulation. We also integrate recent advances in neuro-immuno-endocrinology (e.g., peripheral stress response in the skin) and photo-neuro-immuno-endocrinology, and supplement evidence for stress-cancer crosstalk. Additionally, we clarify the definition of the "risk hub" concept, add a brief literature selection methodology, and propose visualized pathway schematics to enhance clarity. This review provides a refined theoretical foundation for clinical nurses to conduct precise risk stratification, develop pathway-specific intervention plans, and implement personalized care, ultima

Hypertension is a significant preventable risk factor for cardiovascular disease and overall mortality globally, affecting 31.1% of the adult population in 2010. The prevalence of hypertension is rising due to aging and lifestyle factors such as poor diets and insufficient physical activity. Conventional therapy modalities often encompass physical or pharmacological measures; nevertheless, the mental practice of meditation has been employed for centuries to reduce cardiovascular risk. However, the scientific revitalization of this technique has previously prompted doubts over its legitimacy. This paper examines the effects of guided meditations and mindfulness techniques on blood pressure regulation and their potential to enhance cardiac biomarkers, including heart rate variability, cortisol levels, and inflammatory markers, through a review of existing literature and empirical studies. The findings suggest that mindfulness and guided meditation may serve as promising, non-pharmacological complements to traditional hypertension and cardiovascular disease treatments, though further research is needed to strengthen these conclusions.

Poor sleep has been associated with cardiovascular disease (CVD). Research indicates a bidirectional relationship between stress and disrupted sleep. It is possible individual differences in cardiovascular and psychological responses to acute stress may be a pathway connecting sleep and CVD. Research has also separately found biological sex may impact sleep and CVD outcomes. While studies examining subjective sleep and cardiovascular reactivity to acute stress show mixed results, few have concurrently assessed psychological stress responses or considered the moderating role of biological sex. The current paper aimed to explore the associations between subjective sleep quality and cardiovascular and psychological responses to acute stress and the role of biological sex as a potential moderator in this relationship. In two independent studies (Study 1: N = 154, 50.6% female; Study 2: N = 212, 64.2% female), young adults completed a resting baseline period followed by standardized psychological stress tasks with cardiovascular activity measured throughout. Following the stress task, participants rated the intensity and interpretation of their stress during the task. Participants also completed a questionnaire regarding their sleep over the past month. Across both studies, subjective sleep quality was not statistically significantly associated with cardiovascular reactivity (all ps ≥ 0.286, all βs ≤ 0.08). However, worse sleep was significantly associated with increased levels of

Chronic psychological stress refers to repeated or prolonged exposure to adverse social or emotional threats that exceed an individual's adaptive capacity. It is recognized as a risk factor for aging-associated diseases. A growing body of research has shown that there is a link between chronic psychological stress and accelerated aging. Here, we highlight recent findings on the interconnected relationship between chronic psychological stress and major aging hallmarks, including mitochondrial dysfunction, telomere attrition, cellular senescence, epigenetic alterations, inflammation, and genomic instability. We discuss the mechanisms by which chronic psychological stress may drive this effect and explore intervention strategies that could mitigate its adverse effects and promote healthy aging. Moreover, we address current research gaps and propose future research directions to improve our understanding of the intricate relationship between psychological stress and aging.

<h4>Introduction</h4>Psychological stress impairs both mental health and physiological function, making it a major occupational health risk for office workers. Although non-pharmacological emotional interventions have gained attention, scientific evidence for structured animal-based video content remains scarce. This study investigated whether structured puppy video viewing improves stress responses and compared outcomes between normal blood pressure (BP) and elevated BP office workers.<h4>Methods</h4>Sixty-six participants (36 for normal BP, 30 for elevated BP) took part in a non-randomized pre-post intervention, viewing structured puppy videos for 15 min. Systolic BP (SBP), diastolic BP (DBP) and pulse rate were measured as physiological outcomes; psychological outcomes were assessed with the 20-item State Anxiety subscale of the State-Trait Anxiety Inventory (STAI-S) and with the 30-item the Korean Profile of Mood States-Brief (K-POMS-B), summarized as Total Mood Disturbance (TMD).<h4>Results</h4>In normal BP group, SBP decreased by 3.16 mmHg (<i>p</i> = 0.002), pulse rate by 2.76 bpm (<i>p</i> < 0.001), STAI-S by 6.64 points (<i>p</i> < 0.001), and TMD by 7.92 points (<i>p</i> < 0.001) after viewing the video. In the elevated BP group, there were significant reductions in SBP (Δ6.65 mmHg), DBP (Δ4.93 mmHg), pulse rate (Δ4.12 bpm), and STAI-S (Δ9.43 points) (with all <i>p</i> < 0.001), alongside a TMD reduction of 11.77 points (<i>p</i> < 0.001). When comparing between nor

Low cardiovascular reactions to acute psychological stress have been shown among those with substance and non-substance dependencies like exercise dependence. However, associations between exercise dependence and low cardiovascular reactions to stress have been demonstrated between small sex-specific groups with extreme exercise dependence scores. The present study sought to replicate previous findings as well as examine whether exercise dependence across the range of scores was linearly related to reactivity magnitude in a more diverse sample. Participants (n = 161, 65% female) undertook laboratory stress testing. Cardiovascular activity was measured at rest and in response to a 10-min Paced Auditory Serial Addition Test (PASAT). Exercise dependence was measured via three validated questionnaires. There were no significant linear associations between exercise dependence scores and blood pressure reactivity, with or without adjustment for covariates. In a subsample of females aged < 30 years, small negative associations emerged for blood pressure reactivity. Replication analyses of extreme groups created using the EABQ, as in prior work, showed no significant differences in reactivity, but there were some indications of low reactivity among individuals classified as exercise dependent on the EDQ. In conclusion, differences in stress reactivity may not be confined to extreme scoring groups and can also emerge as linear associations. However, the presence and form of these effe

Postoperative cardiovascular complications remain a leading cause of morbidity and mortality after noncardiac surgery, yet current risk models do not incorporate psychosocial stress. With over 300 million noncardiac surgeries performed annually worldwide and a substantial burden of perioperative cardiovascular complications, preoperative chronic stress is increasingly recognized as a potentially modifiable risk factor. Chronic stress produces HPA axis dysregulation, glucocorticoid resistance, sympathetic activation, inflammation, endothelial dysfunction, and hypercoagulability. These pathways overlap with the mechanisms underlying perioperative myocardial injury, arrhythmogenesis, and venous thromboembolism. Prospective data demonstrated that preoperative psychological distress independently predicted 30-day cardiovascular complications and 1-year mortality after noncardiac surgery. Allostatic load studies in noncardiac surgery patients showed that high preoperative physiological burden was associated with up to twofold increases in postoperative mortality and elevated rates of myocardial infarction and venous thromboembolism. Epidemiological evidence further supports that anxiety and depression independently increase cardiovascular risk. Converging evidence suggests that preoperative psychological distress is a relevant perioperative cardiovascular risk factor. However, no randomized controlled trial has evaluated whether targeted preoperative stress reduction can decrease p