Stress-The International Journal on the Biology of Stress最新文献

Stress occurs as a reaction to mental and emotional pressure, anxiety, or scarring. Chronic stress is defined as constant submission to these moments. It can affect several body systems, increase blood pressure, and weaken immunity, thereby interfering with physiological health processes. Thus, this study aims to evaluate the effects of chronic stress on the redox status and histomorphological parameters of salivary glands. Thirty-two albino Wistar male rats were randomly divided into two groups: chronic stress and control. Chronically stressed animals were subjected to a restraint protocol by introducing them into a polyvinyl tube for 4 hours daily for 28 days, allowing immobilization of their movements. Subsequently, the animals were euthanized for further collection of the parotid and submandibular salivary glands. The redox state of the glands was evaluated using the antioxidant capacity against peroxyl radicals (ACAP) and thiobarbituric acid reactive substances (TBARS) assays. Histological analysis was performed through morphometry of the tissues stained with hematoxylin and eosin and histochemical through picrosirius red staining. Both the parotid and submandibular glands of stressed rats exhibited oxidative stress due to a decrease in ACAP and an increase in TBARS levels. However, the parotid glands are more susceptible to harmful changes in the tissue, such as an increase in the stromal area and in the collagen area fraction, decrease in the acinar area, and smaller size of the acinus and ducts. Our results suggest that chronic stress may cause harmful modulation of the redox state of the salivary glands, with different histological repercussions.

Background: Self-reported mental stress is not consistently recognized as a risk factor for stroke. This prompted development of a novel algorithm for stress-phenotype indices to quantify chronic stress prevalence in relation to a modified stroke risk score in a South African cohort. The algorithm is based on biomarkers adrenocorticotrophic hormone, high-density lipoprotein cholesterol, high-sensitive cardiac-troponin-T, and diastolic blood pressure which exemplifies the stress-ischemic-phenotype index. Further modification of the stroke risk score to accommodate alcohol misuse established the stress-diabetes-phenotype index. Whether positive stress-phenotype individuals will demonstrate a higher incidence of stroke in an independent Swedish cohort was unknown and investigated.

Methods: Stress-phenotyping was done at baseline for 50 participants with incident stroke and 100 age-, and sex matched controls (aged 76 ± 5 years) from 2,924 individuals in southern Sweden. The mean time from inclusion to first stroke event was 5 ± 3 years. Stress-phenotyping comparisons and stroke incidence risk were determined.

Results: A positive stress-ischemic-phenotype reflected higher incident stroke (72% vs. 28%, p = 0.019) and mortality rates (41% vs. 23%, p = 0.019). Whereas a positive stress-diabetes-phenotype reflected a higher incident stroke rate (80% vs. 20%, p = 0.008) but similar mortality rate (38% vs. 25%, p = 0.146). Both the positive stress-ischemic (OR: 2.9, 95% CI: 1.3-6.5, p = 0.011) and stress-diabetes-phenotypes (OR: 3.7, 95% CI: 1.5-8.9, p = 0.004) showed large effect size associations with incident stroke independent of cardiovascular risk confounders.

Conclusion: Positive stress-phenotype indices demonstrated a higher incidence of stroke. Ultimately the Malan stress-phenotype algorithms developed in South Africa could confirm incident stroke in an independent Swedish cohort. Stress-phenotyping could thus be useful in clinical routine practice in order to detect individuals at higher stroke risk.

In the current age of technological advancement, stress has emerged as a silent pandemic affecting individuals, especially young generations, globally. Factors such as increased competition, social pressures fueled by social media and smartphones, and a sense of diminished control in the face of modern challenges contribute to rising stress levels. In addition to the negative implications on mental well-being, stress affects physiological processes such as the menstrual cycle. Functional hypogonadotropic hypogonadism is a spectrum ranging ranging from regular menstrual cycles with short or insufficient luteal phases to irregular cycles, oligomenorrhea, anovulation, and complete amenorrhea, depending on how stress variably disrupts gonadotropic-releasing hormone (GnRH) drive. Functional hypothalamic amenorrhea (FHA), the most severe manifestation, is a complex global neuroendocrinopathy with several serious health consequences in addition to amenorrhea and infertility. Concomitant health consequences include bone loss, endothelial dysfunction, and cardiovascular risks. The collective health burden underscores the need for clinical awareness and comprehensive treatment strategies addressing behavioral and biopsychosocial stressors that lead to chronic hypothalamic-pituitary-adrenal (HPA) axis activation. Despite its prevalence and numerous adverse health consequences, research on this condition remains limited, revealing a significant gap in understanding and addressing this condition. Larger and long-term follow-up studies are important to accurately assess FHA prevalence, its health consequences, intervention efficacy, and recovery outcomes.

Burnout is caused by long term psychosocial stress and has, besides the fatigue and mental health burden, been associated with increased risk of adverse physical health, such as for example type 2 diabetes. This study aims to investigate the glucose and insulin levels in individuals with stress related burnout, by assessing these metabolic markers in response to a standard oral glucose tolerance test (OGTT). 38 cases with burnout (13 men and 25 women) and 35 healthy controls (13 men and 22 women) in the age 24-55 were included in the study. The burnout group overall did not differ from healthy controls in glucose or insulin levels during the OGTT. However, the burnout cases who reported more severe burnout symptoms exhibited significantly higher levels of both glucose and insulin levels during the OGTT compared to burnout cases reporting lower severity of symptoms. Furthermore, the group of burnout cases who reported symptoms of depression exhibited higher insulin levels during OGTT compared to the burnout cases without depressive symptoms. The observed higher levels in the burnout cases with most severe symptoms indicate an increased diabetic risk in these patients and it may be of importance to follow glucose and insulin levels in individuals with more severe symptoms of burnout i.e. to perform an OGTT.

Previous reports suggest that the menstrual cycle (MC) phases can impact cortisol concentrations. However, research is needed on whether the MC impacts other markers of stress and immune function. It has also been shown that some biomarkers are impacted by time of day, although differences between morning (AM) and afternoon (PM) biomarkers have not been studied over the course of the MC. This study assessed the effect of MC phases and time of day on salivary stress biomarkers [salivary α-amylase (sAA), secretory immunoglobulin A (SIgA)], progesterone, resting blood pressure and resting heart rate (RHR). A single-group repeated measure design was employed in which seventeen participants (n = 17) monitored their MC for two months while attending eight experimental sessions which included both AM and PM sessions during each predicted 1) menses, 2) follicular, 3) ovulatory and 4) luteal phases. Resting blood pressures, heart rates, body composition parameters (assessed via bioelectrical impedance analysis), sAA and SIgA concentrations were assessed. No time of day x MC phase interactions (p > 0.05) were noted for sAA or SIgA, resting blood pressure, heart rate, or body composition parameters. However, sAA and RHR were significantly higher in the PM, while SIgA was significantly higher in the AM. These data suggest that the MC phases do not impact sAA or SIgA, resting blood pressure, heart rates, or body composition parameters. However, time-of-day impacts RHR and concentrations of sAA and SIgA. These findings provide implications for female participants in research dealing with these biomarkers.

Chronic stress and stress-related mental illnesses such as major depressive disorder (MDD) constitute some of the leading causes of disability worldwide with a higher prevalence in women compared to men. However, preclinical research into stress and MDD is heavily biased toward using male animals only. Aberrant activity of the hypothalamic-pituitary-adrenal (HPA) axis has been linked to the development of MDD and several animal models of MDD have been established based on HPA axis dysregulation. In the present study, we compared stress biomarkers and behavior of male and female mice after acute and chronic restraint stress to investigate potential effects of sex differences in the stress response. Further, the validity of the interrupted repeated restraint stress (IRRS) model as an animal model for the HPA axis disturbances seen in MDD was assessed. After acute stress, female mice showed increased corticosterone secretion and changes in molecular markers suggesting increased HPA axis feedback sensitivity. Acute stress-induced signs of anxiety-like behavior were observed in male mice only suggesting that female mice may be more resilient to the anxiogenic effects of acute stress. Males and females responded similarly to IRRS with no sustained perturbations in HPA axis biomarkers. The IRRS model did not adequately translate to the changes reported in MDD with HPA axis overactivity and more severe perturbation models are likely needed. However, in alignment with previous studies, these data support that there are important sex differences in the HPA axis and that these may contribute to the etiology of stress-related psychiatric disorders.

Recent years brought considerable attention to the connection between chronic stress and the development of autoimmune diseases. However, little is still known about the impact of prolonged stress reactions on the onset and course of primary Sjögren Syndrome (pSS). This study aimed to seek for associations between chronic stress, resulting from stressful life events, and pSS. In the study, 50 patients with diagnosed pSS, as well as 50 control patients with osteoarthritis underwent an assessment. Modified Holmes-Rahe (H-R) stress scale was used in order to evaluate the impact of stressful events within 12 months prior to the diagnosis. Patients with pSS had a significantly higher total score on H-R stress scale within one-year preceding the disease diagnosis (152 ± 66.3 vs 50 ± 54.6; p $<$ 0.001). Additionally, the pSS patients more commonly than the controls reported a subjectively perceived correlation between stressful events and the occurrence of disease symptoms (50% vs 12%; p $<$ 0.001). Moreover, the H-R score at the time of the assessment correlated with the disease activity. The results support the view that pSS belongs to the group of diseases which pathogenesis is closely related to stressful life events. The novelty of this work lies in focus on both the correlation of stress on the onset of autoimmune disease as well as the activity of previously diagnosed disorder. Our data contributes to finding evidence-based medicine (EBM) arguments to what has until recently been merely a thematic observation-the harmfulness of negative stress on individual's health status.

Chronic stress leads to hypofunction of the medial prefrontal cortex (mPFC), mechanisms of which remain to be determined. Enhanced activation of GABAergic of parvalbumin (PV) expressing interneurons (INs) is thought to play a role in stress-induced prefrontal inhibition. In this study, we tested whether chemogenetic inhibition of mPFC PV INs after chronic stress can rescue chronic stress-related behavioral and physiological phenotypes. Mice underwent 2 weeks of chronic variable stress (CVS) followed by a battery of behavioral tests known to be affected by chronic stress exposure, e.g. an open field (OF), novel object recognition (NOR), tail suspension test (TST), sucrose preference test (SPT), and light dark (LD) box. Inhibitory DREADDs were actuated by 3 mg/kg CNO administered 30 min prior to each behavioral test. CVS caused hyperactivity in the OF, reduced sucrose preference in the SPT (indicative of enhanced anhedonia), and increased anxiety-like behavior in the LD box. Inhibition of PV IN after stress mitigated these effects. In addition, CVS also resulted in reduced thymus weight and body weight loss, which were also mitigated by PV IN inhibition. Our results indicate that chronic stress leads to plastic changes in PV INs that may be mitigated by chemogenetic inhibition. Our findings implicate cortical GABAergic INs as a therapeutic target in stress-related diseases.

Stress is an established risk factor for negative health outcomes. Salivary cortisol and testosterone concentrations increase in response to acute psychosocial stress. It's crucial to reduce stress for health and well-being through evidence-based interventions. Body-mind interventions such as meditation and Tai Chi have shown reduced cortisol levels but mixed results in testosterone concentration after stress. To address this research gap, we conducted a pilot randomized controlled trial to examine the modulating effects of a short-term (seven 20-minute sessions) mindfulness meditation on testosterone and cortisol in response to acute stress. Using one form of mindfulness meditation - Integrative Body-Mind Training (IBMT) and an active control-relaxation training (RT), we assessed salivary cortisol and testosterone concentrations at three stages of stress intervention - rest, stress, and an additional 20-min IBMT or RT practice. We found increased cortisol and testosterone concentrations after acute stress in both groups, but testosterone rise was not associated with cortisol rise. Moreover, an additional practice immediately after stress produced higher testosterone concentrations in the IBMT group than the RT group, whereas cortisol concentration increased in the RT group than in the IBMT group at the same time point. These findings indicate that brief mindfulness intervention modulates a dual-hormone profile of testosterone and cortisol in response to acute stress presumably via the co-regulation of hypothalamus-pituitary-adrenal and hypothalamus-pituitary-testicular axes.

Chronic stress exposure during development can have lasting behavioral consequences that differ in males and females. More specifically, increased depressive behaviors in females, but not males, are observed in both humans and rodent models of chronic stress. Despite these known stress-induced outcomes, the molecular consequences of chronic adolescent stress in the adult brain are less clear. The stress hormone corticosterone activates the glucocorticoid receptor, and activity of the receptor is regulated through interactions with co-chaperones-such as the immunophilin FK506 binding proteins 5 (FKBP5). Previously, it has been reported that the adult stress response is modified by a history of chronic stress; therefore, the current study assessed the impact of chronic adolescent stress on the interactions of the glucocorticoid receptor (GR) with its regulatory co-chaperone FKBP5 in response to acute stress in adulthood. Although protein presence for FKBP5 did not differ by group, assessment of GR-FKBP5 interactions demonstrated that adult females with a history of chronic adolescent stress had elevated GR-FKBP5 interactions in the hippocampus following an acute stress challenge which could potentially contribute to a reduced translocation pattern given previous literature describing the impact of FKBP5 on GR activity. Interestingly, the altered co-chaperone interactions of the GR in the stressed female hippocampus were not coupled to an observable difference in transcription of GR-regulated genes. Together, these studies show that chronic adolescent stress causes lasting changes to co-chaperone interactions with the glucocorticoid receptor following stress exposure in adulthood and highlight the potential role that FKBP5 plays in these modifications. Understanding the long-term implications of adolescent stress exposure will provide a mechanistic framework to guide the development of interventions for adult disorders related to early life stress exposures.