976 resultados para PSYCHOSOCIAL STRESS


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Hypertension is a known risk factor for cardiovascular disease. Hypertensive individuals show exaggerated norepinephrine (NE) reactivity to stress. Norepinephrine is a known lipolytic factor. It is unclear if, in hypertensive individuals, stress-induced increases in NE are linked with the elevations in stress-induced circulating lipid levels. Such a mechanism could have implications for atherosclerotic plaque formation. In a cross-sectional, quasi-experimentally controlled study, 22 hypertensive and 23 normotensive men (mean +/- SEM, 45 +/- 3 years) underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma NE and the plasma lipid profile (total cholesterol [TC], low-density-lipoprotein cholesterol [LDL-C], high-density-lipoprotein cholesterol, and triglycerides) immediately before and after stress and at 20 and 60 minutes of recovery. All lipid levels were corrected for stress hemoconcentration. Compared with normotensives, hypertensives had greater TC (P = .030) and LDL-C (P = .037) stress responses. Independent of each other, mean arterial pressure (MAP) upon screening and immediate increase in NE predicted immediate stress change in TC (MAP: beta = .41, P = .003; NE: beta = .35, P = .010) and LDL-C (MAP: beta = .32, P = .024; NE: beta = .38, P = .008). Mean arterial pressure alone predicted triglycerides stress change (beta = .32, P = .043) independent of NE stress change, age, and BMI. The MAP-by-NE interaction independently predicted immediate stress change of high-density-lipoprotein cholesterol (beta = -.58, P < .001) and of LDL-C (beta = -.25, P < .08). We conclude that MAP and NE stress reactivity may elicit proatherogenic changes of plasma lipids in response to acute psychosocial stress, providing one mechanism by which stress might increase cardiovascular risk in hypertension.

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Little is known about the influence of different stressors on fine motor skills, the concentration of testosterone (T), and their interaction in adolescents. Therefore, 62 high school students aged 14–15 years were randomly assigned to two experimental groups (exercise, psychosocial stress) and a control group. Exercise stress was induced at 65–75% of the maximum heart rate by running for 15 minutes (n = 24). Psychosocial stress was generated by an intelligence test (HAWIK- IV), which was uncontrollable and characterized by social-evaluative-threat to the students (n=21). The control group followed was part of a regular school lesson with the same duration (n = 28). Saliva was collected after a normal school lesson (pre-test) as well as after the intervention/control period (post-test) and was analyzed for testosterone. Fine motor skills were assessed pre- and post-intervention using a manual dexterity test (Flower Trail) from the Movement Assessment Battery for Children-2. A repeated measure ANCOVA including gender as a covariate revealed a significant group by test interaction, indicating an increase in manual dexterity only for the psychosocial stress group. Correlation analysis of all students shows that the change of testosterone from pre- to post-test was directly linked (r = 2.31, p = .01) to the changes in manual dexterity performance. Participants showing high increases in testosterone from pre- to post-test made fewer mistakes in the fine motor skills task. Findings suggest that manual dexterity increases when psychosocial stress is induced and that improvement of manual dexterity performance corresponds with the increase of testosterone.

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BACKGROUND The presence of social support has been associated with decreased stress responsiveness. Recent animal studies suggest that the neuropeptide oxytocin is implicated both in prosocial behavior and in the central nervous control of neuroendocrine responses to stress. This study was designed to determine the effects of social support and oxytocin on cortisol, mood, and anxiety responses to psychosocial stress in humans. METHODS In a placebo-controlled, double-blind study, 37 healthy men were exposed to the Trier Social Stress Test. All participants were randomly assigned to receive intranasal oxytocin (24 IU) or placebo 50 min before stress, and either social support from their best friend during the preparation period or no social support. RESULTS Salivary free cortisol levels were suppressed by social support in response to stress. Comparisons of pre- and poststress anxiety levels revealed an anxiolytic effect of oxytocin. More importantly, the combination of oxytocin and social support exhibited the lowest cortisol concentrations as well as increased calmness and decreased anxiety during stress. CONCLUSIONS Oxytocin seems to enhance the buffering effect of social support on stress responsiveness. These results concur with data from animal research suggesting an important role of oxytocin as an underlying biological mechanism for stress-protective effects of positive social interactions.

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It has been previously shown that the implicit affiliation motive – the need to establish and maintain friendly relationships with others – leads to chronic health benefits. The underlying assumption for the present research was that the implicit affiliation motive also moderates the salivary cortisol response to acute psychological stress when some aspects of social evaluation and uncontrollability are involved. By contrast we did not expect similar effects in response to exercise as a physical stressor. Fifty-nine high school students aged M = 14.8 years were randomly assigned to a psychosocial stress (publishing the results of an intelligence test performed), a physical stress (exercise intensity of 65–75% of HRmax), and a control condition (normal school lesson) each lasting 15 min. Participants’ affiliation motives were assessed using the Operant Motive Test and salivary cortisol samples were taken pre and post stressor. We found that the strength of the affiliation motive negatively predicted cortisol reactions to acute psychosocial but not to physical stress when compared to a control group. The results suggest that the affiliation motive buffers the effect of acute psychosocial stress on the HPA axis.

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Flavanoid-rich dark chocolate consumption benefits cardiovascular health, but underlying mechanisms are elusive. We investigated the acute effect of dark chocolate on the reactivity of prothrombotic measures to psychosocial stress. Healthy men aged 20-50 years (mean ± SD: 35.7 ± 8.8) were assigned to a single serving of either 50 g of flavonoid-rich dark chocolate (n=31) or 50 g of optically identical flavonoid-free placebo chocolate (n=34). Two hours after chocolate consumption, both groups underwent an acute standardised psychosocial stress task combining public speaking and mental arithmetic. We determined plasma levels of four stress-responsive prothrombotic measures (i. e., fibrinogen, clotting factor VIII activity, von Willebrand Factor antigen, fibrin D-dimer) prior to chocolate consumption, immediately before and after stress, and at 10 minutes and 20 minutes after stress cessation. We also measured the flavonoid epicatechin, and the catecholamines epinephrine and norepinephrine in plasma. The dark chocolate group showed a significantly attenuated stress reactivity of the hypercoagulability marker D-dimer (F=3.87, p=0.017) relative to the placebo chocolate group. Moreover, the blunted D-dimer stress reactivity related to higher plasma levels of the flavonoid epicatechin assessed before stress (F=3.32, p = 0.031) but not to stress-induced changes in catecholamines (p's=0.35). There were no significant group differences in the other coagulation measures (p's≥0.87). Adjustments for covariates did not alter these findings. In conclusion, our findings indicate that a single consumption of flavonoid-rich dark chocolate blunted the acute prothrombotic response to psychosocial stress, thereby perhaps mitigating the risk of acute coronary syndromes triggered by emotional stress.

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Anticipatory cognitive stress appraisal (ACSA) can affect the stress-induced release of stress hormones, which, in turn, can modulate microbicidal potential of macrophages. This study examines whether ACSA modulates wound-induced activation of macrophage microbicidal potential in 22 acutely stressed compared to 17 nonstressed healthy men. After catheter-induced wound infliction and completing the ACSA questionnaire, the stress group underwent an acute mental stress task, while the nonstressed group did not. Macrophage microbicidal potential and stress hormones were repeatedly measured. In acutely stressed men, but not in nonstressed men, higher scores in ACSA related to lower macrophage microbicidal potential. This association was statistically mediated by the norepinephrine (NE) stress response. Our data suggest that ACSA modulates stress-induced suppression of wound-induced macrophage activation and that the NE stress response underlies this effect.

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Empathy is a core prerequisite for human social behavior. Relatively, little is known about how empathy is influenced by social stress and its associated neuroendocrine alterations. The current study was designed to test the impact of acute stress on emotional and cognitive empathy. Healthy male participants were exposed to a psychosocial laboratory stressor (trier social stress test, (TSST)) or a well-matched control condition (Placebo-TSST). Afterwards they participated in an empathy test measuring emotional and cognitive empathy (multifaceted empathy test, (MET)). Stress exposure caused an increase in negative affect, a rise in salivary alpha amylase and a rise in cortisol. Participants exposed to stress reported more emotional empathy in response to pictures displaying both positive and negative emotional social scenes. Cognitive empathy (emotion recognition) in contrast did not differ between the stress and the control group. The current findings provide initial evidence for enhanced emotional empathy after acute psychosocial stress.

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Today, health problems are likely to have a complex and multifactorial etiology, whereby psychosocial factors interact with behaviour and bodily responses. Women generally report more health problems than men. The present thesis concerns the development of women’s health from a subjective and objective perspective, as related to psychosocial living conditions and physiological stress responses. Both cross-sectional and longitudinal studies were carried out on a representative sample of women. Data analysis was based on a holistic person-oriented approach as well as a variable approach. In Study I, the women’s self-reported symptoms and diseases as well as self-rated general health status were compared to physician-rated health problems and ratings of the general health of the women, based on medical examinations. The findings showed that physicians rated twice as many women as having poor health compared to the ratings of the women themselves. Moreover, the symptom ”a sense of powerlessness” had the highest predictive power for self-rated general health. Study II investigated individual and structural stability in symptom profiles between adolescence and middle-age as related to pubertal timing. There was individual stability in symptom reporting for nearly thirty years, although the effect of pubertal timing on symptom reporting did not extend into middle-age. Study III explored the longitudinal and current influence of socioeconomic and psychosocial factors on women’s self-reported health. Contemporary factors such as job strain, low income, financial worries, and double exposure in terms of high job strain and heavy domestic responsibilities increased the risk for poor self-reported health in middle-aged women. In Study IV, the association between self-reported symptoms and physiological stress responses was investigated. Results revealed that higher levels of medically unexplained symptoms were related to higher levels of cortisol, cholesterol, and heart rate. The empirical findings are discussed in relation to existing models of stress and health, such as the demand-control model, the allostatic load model, the biopsychosocial model, and the multiple role hypothesis. It was concluded that women’s health problems could be reduced if their overall life circumstances were improved. The practical implications of this might include a redesign of the labour market giving women more influence and control over their lives, both at and away from work.

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This study investigated the effect of a fear-based personality trait, as conceptualised in Gray’s revised reinforcement sensitivity theory (RST) by the strength of the fight/flight/freeze system (FFFS), on young people’s driving simulator performance under induced psychosocial stress. Seventy-one young drivers completed the Jackson-5 questionnaire of RST traits, followed by a psychosocial stress or relaxation induction procedure (random allocation to groups) and then a city driving simulator task. Some support was found for the hypothesis that higher FFFS sensitivity would result in poorer driving performance under stress, in terms of significantly poorer hazard responses, possibly due to an increased attentional focus on the aversive cues inherent in the stress induction leaving reduced attentional capacity for the driving task. These results suggest that stress may lead to riskier driving behaviour in individuals with fearful RST personality styles.

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This chapter presents a pilot study examining the interactive contributions of executive function development/impairment and psychosocial stress to young adults’ (17-30 years old) driving behaviour in a simulator city scenario.

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The model of developmental origins of health and disease proposes that organisms during fetal period utilize cues that enable their adaptation in the postnatal environment they are likely to live, having short-term advantages when trying to survive in environment but simultaneously in the long run have costs for health. A large body of epidemiological research has found that low birth weight, a marker of intrauterine conditions, is associated with cardiovascular (CV) disease. Since the reported associations of birth weight with normal variation in the resting blood pressure (BP), a major predictor of CV disease risk, have been modest, a key candidate mediating the link has been CV and hypothalamus-pituitary-adrenal axes (HPAA) reactivity to stress. In addition, not only weight at birth but also gestational age and early postnatal growth may have independent associations to stress reactivity. The aim of this thesis was to investigate whether pre- and postnatal growth and gestational age are associated with CV and HPAA activity before, during and after stress in childhood and in late adulthood. Altogether 287 men and women aged 60-70 and 299 boys and girls aged 7-9 underwent Trier Social Stress Test. Several indices of HPAA and CV were measured and birth size and gestational age were obtained from birth records. Results showed that low birth weight was associated with low HPAA activity during psychosocial stress, and rapid gain in BMI during years 7-11 was related to heightened stress reactivity to psychosocial stress. Size at birth in children and gestational age and early postnatal (0-2 years) gain in height in adults were associated with CV stress responses; however, in a sex-specific manner. Given that CV stress responses and HPAA activity are markers of CV disease vulnerability, our results may partly explain the associations between early environment and later CV disease.