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

Acute stress causes a shift from executive to automated behavior. A key executive function suffering from this shift is working memory. Working memory is mainly negatively affected in the first 10 and more than 25 minutes after acute stress. These phases coincide with increased central levels of noradrenaline and cortisol. Increased levels of both hormones can cause a relative deactivation in prefrontal areas related to working memory processing. However, so far, there is little research that investigates the complete relationship between acute stress and resulting changes in stress hormones, neural activation, and working memory processing, over time. In this study, we used functional near-infrared spectroscopy to measure prefrontal activity during an nback task in a stress (28 subjects, 7 female/21 male) and a control group (28 subjects, 10 female/18 male) once (20 minutes) before and twice (4 and 24 minutes) after a socially evaluated cold pressor test or a warm water control condition. Additionally, we regularly measured changes in salivary cortisol and α-amylase (a correlate of central noradrenaline) during the experiment. While salivary cortisol was increased starting 14 minutes after acute stress, no effect of stress on salivary α-amylase or working memory performance was found. On a neural level, we found a marginally stronger decline in 3-back-related prefrontal activity from the first to the third measurement point in the stress than in the control group. These results present tentative evidence for a negative effect of acute stress on working-memory-related prefrontal processing mediated by central cortisol levels.

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.

Prenatal stress has been associated with poor cognitive outcomes in offspring, but the evidence about the role of exact timing of exposure is mixed and that about causal mechanisms is limited. Using the Avon Longitudinal Study of Parents and Children, this study (N = 4,525) explored the role of inflammation in the association between timing of prenatal-stressor exposure and cognitive functioning in middle childhood (ages 9-11 years). Prenatal-stressor exposure was measured at two timepoints (until 18 weeks gestation and from then until 8 weeks postpartum). Cognitive outcomes included working memory, spelling, reading (speed, accuracy, comprehension), response inhibition, selective attention, attentional control, social cognition, and verbal ability. Path models examined mediation via inflammatory markers (IL-6 and CRP, at age 9 years), and factor analysis on the outcomes identified broad cognitive domains. The findings from regression models controlling for confounders and mutually adjusting for early and later prenatal-stressor exposure suggest that early prenatal events impacted only reading comprehension. Later-prenatal events had a detrimental effect on response inhibition, social cognition, and verbal ability, but a seemingly beneficial effect on reading accuracy and comprehension, likely due to suppression. Early prenatal events had no impact on the broad domains identified by factor analysis (reading/spelling, attention, and social communication), but later-prenatal events were inversely associated with both reading/spelling and social communication. Inflammation did not mediate prenatal-stressor effects on either broad domains or specific outcomes. It appears that stressor exposure later rather than early in gestation impacted children's reading/spelling and social communication. There was no evidence that inflammation mediated that impact.

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.

Stress-induced neuropsychiatric disorders are among the most prevalent medical conditions and have widespread effects on both patients and society. Females experience over twice the rates of stress-related anxiety and depression when compared to males and often exhibit worse symptomatology and treatment outcomes. However, preclinical experiments exploring the neurobiological mechanisms of stress susceptibility in females have been traditionally understudied. Previous data from our lab has determined that females are selectively vulnerable to the consequences of vicarious witness stress, and these experiments were designed to determine specific behavioral and physiological factors that could predict which groups would be more susceptible to the effects of stress. Adult, female, Sprague-Dawley rats were first exposed to a ferret predator odor to determine baseline individual differences in behavioral responses. Rats were stratified by the duration of freezing behavior exhibited in response to the ferret odor and equally balanced into non-stressed controls and vicarious witness stress exposed groups. These female rats were then assessed on a battery of behavioral tasks including sucrose preference, elevated plus maze, acoustic startle, and the ferret odor and witness stress cue exposures to determine if baseline differences in stress responding can predict the behavioral response to future stress and stress cues. High freezing in response to the ferret odor was associated with behavioral sensitization to witness stress and hypervigilant responses to stress cues that was accompanied by exaggerated neuroimmune responses. These experiments establish a powerful behavioral predictor of stress susceptibility in females and begin to address neurobiological correlates that underlie this response.

Music listening may decrease pain via psychobiological mechanisms. Music listening style (MLS) influences music processing: Music empathizers (ME) focus on emotional aspects of music, whereas music systemizers (MS) focus on structural aspects, potentially affecting processes of music-induced analgesia. The effects of the MLS on music-induced analgesia might depend on the source of music selection (i.e. who selects the music) and gender. Different psychological mechanisms, such as stimulus-induced emotions and subjective stress, might mediate the effects of an empathizing versus systemizing MLS on pain. The purpose of this study was (a) to test how MLS influences pain during music listening, depending on the source of music selection and gender, and (b) to explore underlying psychological mechanisms. 61 participants (age: M = 24.23, SD = 3.85; four groups: male/female ME/MS) listened to stimuli (participant-selected/researcher-selected music/control) during cold pressor tests. Pain intensity, pain tolerance, and psychological mechanisms (stimulus-induced emotions, subjective stress) were repeatedly measured. Multilevel and mediation analyses were conducted. The MLS did not directly influence pain, but female ME were most pain sensitive with participant-selected music. Pain was tolerated longest for participant-selected music. The effect of MLS on pain intensity was not mediated by stimulus-induced emotions but by subjective stress. Our results indicate that music increases pain tolerance the most when participants select it. However, we found initial evidence that women scoring high on ME show increased pain when listening to their self-selected music. We also found initial evidence for the importance of subjective stress as a potential mechanism in the context of music-based pain management.

To survive predation, animals must be able to detect and appropriately respond to predator threats in their environment. Such defensive behaviors are thought to utilize hard-wired neural circuits for threat detection, sensorimotor integration, and execution of ethologically-relevant behaviors. Despite being hard-wired, defensive behaviors (i.e. fear responses) are not fixed, but rather show remarkable flexibility, suggesting that extrinsic factors such as threat history, environmental contexts, and physiological state may alter innate defensive behavioral responses. The goal of the present study was to examine how extrinsic and intrinsic factors influence innate defensive behaviors in response to visual threats. In the absence of a protective shelter, our results indicate that mice showed robust freezing behavior following both looming (proximal) and sweeping (distal) threats, with increased behavioral vigor in response to looming stimuli, which represent a higher threat imminence. Repeated presentation of looming or sweeping stimuli at short inter-trial intervals resulted in robust habituation of freezing, which was accelerated at longer inter-trial intervals, regardless of contextual cues. Finally, prior stress history such as acute foot shock further disrupted innate freezing habituation, resulting in a delayed habituation phenotype, consistent with a heightened fear state. Together, our results indicate that extrinsic factors such as threat history, environmental familiarity, and stressors have robust and diverse effects on defensive behaviors, highlighting the behavioral flexibility in how mice respond to predator threats.

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.