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

Research on stress has demonstrated that the hypothalamic-pituitary-adrenal (HPA) axis contributes to major depressive disorder in youth. Hair glucocorticoids are key biological markers of chronic stress. We assessed group differences in hair cortisol and cortisone concentrations, and the cortisol/cortisone ratio between depressed adolescent women and a non-depressed comparison group. Further, within the depression group, we explored the contribution of symptom severity and clinical correlates of depression in relation to glucocorticoid concentrations. Hair samples of three centimeters for 74 adolescent women (41 in the depression group and 33 in the comparison group), aged between 12 and 19 years old, were analyzed. Depressive and anxiety symptoms were measured using the Beck Youth Inventory II and clinical correlates of depression were measured using the Childhood Trauma Questionnaire-Short Form and the Borderline Personality Features Scale for Children. No significant differences emerged between the depression group and the comparison group on hair cortisol or hair cortisone concentrations. However, groups differed significantly on the cortisol/cortisone ratio, a proposed proxy of 11-beta-hydroxysteroid dehydrogenase activity, with a higher ratio for the depression group. Within the depression group, neither symptom severity nor clinical correlates were associated with glucocorticoid concentrations. Although cross-sectional, our findings highlight the importance of future studies to test whether the group difference found in cortisol/cortisone ratio is the result of alterations in 11-beta-hydroxysteroid dehydrogenase enzymes (type 1 or 2) activity. Further research is thus needed to clarify the role of these enzymes in major depressive disorder in youth and to develop more targeted intervention strategies.

Depression commonly accompanies acute coronary syndrome (ACS), impacting up to 30% of patients and correlating with adverse outcomes. Our study aimed to assess the accuracy of clinical impression compared to the PHQ9 questionnaire for evaluating depression in ACS patients admitted to the cardiac intensive care unit. Screening for depression was conducted at least 48 hours from hospital admission and 24 hours following coronary angiography and PCI. The assessment was performed separately and in a blinded manner by the clinical assessment of the attending medical team and by the PHQ9 questionnaire. The study comprised 150 ACS patients with a mean age of 62 ± 13 years. Baseline clinical and demographic characteristics were typical for ACS patients. Based on the PHQ9 questionnaire, depressive symptoms were above the cutoff for clinical depression in 31 (20.7%) patients, with 10 (32.3%) of them experiencing moderate or severe depression (PHQ9 score >15). There were no significant differences in clinical baseline characteristics between the groups with and without clinical depression. Compared to the PHQ9 questionnaire, the medical team's assessment of depression demonstrated a reasonable specificity of 84% and low sensitivity of 32%. Negative and positive predictive values were 82.6% and 35.8%, respectively. Similar findings were observed in subgroup analyses according to gender, age, type of ACS, and history of cardiovascular disease. Depression is prevalent among ACS patients, highlighting the importance of an increased awareness of this condition. Our findings suggest that detecting clinically significant severity of depressive symptoms by the attending medical team alone may not suffice for depression assessment. Incorporating validated screening tools such as the PHQ9 questionnaire or involving psychological evaluations can enhance the accuracy of depression diagnosis in ACS patients. This multifaceted approach is crucial for ensuring comprehensive care and improving patient outcomes.

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.

Present study was aimed to elucidate the role of corticotropin releasing hormone (CRH) neurons located in the paraventricular nucleus of the hypothalamus (PVN) in the mechanisms of stress-induced insomnia. Experiments were done in the rodent model of traumatic stress, mice exposure to the predator (rat) odor. Sleep changes associated with this model of stress were first assessed in adult male C57BL/6J wild-type mice (n = 12). The effect of chemogenetic silencing of CRH neurons within the PVN on traumatic stress-induced insomnia was examined in adult male CRH-ires-Cre mice using designer receptors exclusively activated by designer drugs (DREADD) technology. Animals received bilateral injections of inhibitory DREADD vector AAV-hSyn-DIO-hM4Di-mCherry (n = 10) or control AAV-hSyn-DIO-mCherry virus (n = 10) into the PVN during surgery. The DREADD was activated by intraperitoneal injection of clozapine-N-oxide (CNO) prior to the induction of traumatic stress. The exposure of mice to rat odor induced strong long-lasting suppression of both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep stages in both experiments. Selective suppression of CRH neurons within the PVN alleviated acute insomnia by significantly increasing the time spent in NREM sleep but it did not counteract the stress-induced deficit in REM sleep. These findings suggest a specific role for CRH-secreting neurons within the PVN in the suppression of NREM sleep during acute insomnia caused by predator odor stress, whereas REM sleep suppression is controlled by a different mechanism.

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.