Concept: Acute stress reaction
- Proceedings of the National Academy of Sciences of the United States of America
- Published about 5 years ago
We compared the impact of media vs. direct exposure on acute stress response to collective trauma. We conducted an Internet-based survey following the Boston Marathon bombings between April 29 and May 13, 2013, with representative samples of residents from Boston (n = 846), New York City (n = 941), and the remainder of the United States (n = 2,888). Acute stress symptom scores were comparable in Boston and New York [regression coefficient (b) = 0.43; SE = 1.42; 95% confidence interval (CI), -2.36, 3.23], but lower nationwide when compared with Boston (b = -2.21; SE = 1.07; 95% CI, -4.31, -0.12). Adjusting for prebombing mental health (collected prospectively), demographics, and prior collective stress exposure, six or more daily hours of bombing-related media exposure in the week after the bombings was associated with higher acute stress than direct exposure to the bombings (continuous acute stress symptom total: media exposure b = 15.61 vs. direct exposure b = 5.69). Controlling for prospectively collected prebombing television-watching habits did not change the findings. In adjusted models, direct exposure to the 9/11 terrorist attacks and the Sandy Hook School shootings were both significantly associated with bombing-related acute stress; Superstorm Sandy exposure wasn’t. Prior exposure to similar and/or violent events may render some individuals vulnerable to the negative effects of collective traumas. Repeatedly engaging with trauma-related media content for several hours daily shortly after collective trauma may prolong acute stress experiences and promote substantial stress-related symptomatology. Mass media may become a conduit that spreads negative consequences of community trauma beyond directly affected communities.
Stress research has progressively become more integrative in nature, seeking to unfold crucial relations between the different phenotypic levels of stress manifestations. This study sought to unravel stress-induced variations in expression of human microRNAs sampled in peripheral blood mononuclear cells and further assess their relationship with neuronal and psychological indices. We obtained blood samples from 49 healthy male participants before and three hours after performing a social stress task, while undergoing functional magnetic resonance imaging (fMRI). A seed-based functional connectivity (FC) analysis was conducted for the ventro-medial prefrontal cortex (vmPFC), a key area of stress regulation. Out of hundreds of microRNAs, a specific increase was identified in microRNA-29c (miR-29c) expression, corresponding with both the experience of sustained stress via self-reports, and alterations in vmPFC functional connectivity. Explicitly, miR-29c expression levels corresponded with both increased connectivity of the vmPFC with the anterior insula (aIns), and decreased connectivity of the vmPFC with the left dorso-lateral prefrontal cortex (dlPFC). Our findings further revealed that miR-29c mediates an indirect path linking enhanced vmPFC-aIns connectivity during stress with subsequent experiences of sustained stress. The correlative patterns of miR-29c expression and vmPFC FC, along with the mediating effects on subjective stress sustainment and the presumed localization of miR-29c in astrocytes, together point to an intriguing assumption; miR-29c may serve as a biomarker in the blood for stress-induced functional neural alterations reflecting regulatory processes. Such a multi-level model may hold the key for future personalized intervention in stress psychopathology.
To assess the prevalence of symptoms of acute stress reactions (ASR) and post-traumatic stress disorder (PTSD) in paediatric trainees following their involvement in child death.
The experience of driving has been suggested to be detrimental to health. One hypothesis is that each exposure elicits an acute stress response, and that repeated exposures may act as a chronic stressor.
The role of repeated exposure to collective trauma in explaining response to subsequent community-wide trauma is poorly understood. We examined the relationship between acute stress response to the 2013 Boston Marathon bombings and prior direct and indirect media-based exposure to three collective traumatic events: the September 11, 2001 (9/11) terrorist attacks, Superstorm Sandy, and the Sandy Hook Elementary School shooting. Representative samples of residents of metropolitan Boston (n = 846) and New York City (n = 941) completed Internet-based surveys shortly after the Boston Marathon bombings. Cumulative direct exposure and indirect exposure to prior community trauma and acute stress symptoms were assessed. Acute stress levels did not differ between Boston and New York metropolitan residents. Cumulative direct and indirect, live-media-based exposure to 9/11, Superstorm Sandy, and the Sandy Hook shooting were positively associated with acute stress responses in the covariate-adjusted model. People who experience multiple community-based traumas may be sensitized to the negative impact of subsequent events, especially in communities previously exposed to similar disasters.
The majority of patients with epilepsy report that seizures are sometimes triggered or provoked. Stress is the most frequently self-reported seizure-precipitant. The mechanisms underlying stress-sensitivity of seizures are currently unresolved. We hypothesized that stress-sensitivity of seizures relates to alteration of the stress response, which could affect neuronal excitability and hence trigger seizures. To study this, children with epilepsy between 6 and 17 years of age and healthy controls, with similar age, sex and intelligence, were exposed to a standardized acute psychosocial stressor (the Trier Social Stress Test for Children), during which salivary cortisol and sympathetic parameters were measured. Beforehand, the relation between stress and seizures in children with epilepsy was assessed by (i) a retrospective questionnaire; and (ii) a prospective 6-week diary on stress and seizure occurrence. Sixty-four children with epilepsy and 40 control subjects were included in the study. Of all children with epilepsy, 49% reported that seizures were precipitated by acute stress. Diary analysis showed a positive association between acute stress and seizures in 62% of children who experienced at least one seizure during the diary period. The acute social stress test was completed by 56 children with epilepsy and 37 control subjects. Children with sensitivity of seizures for acute stress, either determined by the questionnaire or by the prospective diary, showed a blunted cortisol response to stress compared with patients without acute stress-precipitated seizures and healthy controls (questionnaire-based F = 2.74, P = 0.018; diary-based F = 4.40, P = 0.007). No baseline differences in cortisol were observed, nor differences in sympathetic stress response. The relation between acute stress-sensitivity of seizures and the cortisol response to stress remained significant in multivariable analysis (β = -0.30, P = 0.03). Other variables associated with the acute stress response were the number of anti-epileptic drugs (β = -0.27, P = 0.05) and sleep quality (β = 0.30, P = 0.03). In conclusion, we show that children with acute stress-sensitive seizures have a decreased cortisol response to stress. These results support our hypothesis that stress-sensitivity of seizures is associated with alterations of the stress response, thereby providing a first step in unravelling the mechanisms behind the seizure-precipitating effects of stress. Increased knowledge of the relation between stress and seizures in childhood epilepsy might benefit our understanding of the fundamental processes underlying epilepsy and ictogenesis in general, and provide valuable clues to direct the development of new therapeutic strategies for epilepsy.
- The British journal of psychiatry : the journal of mental science
- Published about 5 years ago
Although youths in many countries have been exposed to terrorism, few studies have examined early risk and protective factors for the subsequent development of mental health problems.
The acute stress response functions to prioritize behavioural and physiological processes that maximize survival in the face of immediate threat. There is variation between individuals in the strength of the adult stress response that is of interest in both evolutionary biology and medicine. Age is an established source of this variation-stress responsiveness diminishes with increasing age in a range of species-but unexplained variation remains. Since individuals of the same chronological age may differ markedly in their pace of biological ageing, we asked whether biological age-measured here via erythrocyte telomere length-predicts variation in stress responsiveness in adult animals of the same chronological age. We studied two cohorts of European starlings in which we had previously manipulated the rate of biological ageing by experimentally altering the competition experienced by chicks in the fortnight following hatching. We predicted that individuals with greater developmental telomere attrition, and hence greater biological age, would show an attenuated corticosterone (CORT) response to an acute stressor when tested as adults. In both cohorts, we found that birds with greater developmental telomere attrition had lower peak CORT levels and a more negative change in CORT levels between 15 and 30 min following stress exposure. Our results, therefore, provide strong evidence that a measure of biological age explains individual variation in stress responsiveness: birds that were biologically older were less stress responsive. Our results provide a novel explanation for the phenomenon of developmental programming of the stress response: observed changes in stress physiology as a result of exposure to early-life adversity may reflect changes in ageing.
- Journal of child psychology and psychiatry, and allied disciplines
- Published over 2 years ago
The revision of Acute Stress Disorder (ASD) in the DSM-5 (DSM-5, 2013) proposes a cluster-free model of ASD symptoms in both adults and youth. Published evaluations of competing models of ASD clustering in youth have rarely been examined.
Driving may be detrimental to health, with one hypothesis suggesting that driving may elicit an acute stress response and, with repeated exposures, may become a chronic stressor. The present study examined the stress response to driving and the effectiveness of a prior exercise bout in dampening this response. Twenty healthy adults performed three tasks: control, driving and exercise plus driving. Heart rate (HR), heart rate variability (HRV), blood pressure (BP) and cortisol were measured to quantify the acute stress response to each condition. Data indicated a stress response to driving: HR was elevated and HRV was reduced during the driving task compared with control. HR was elevated and HRV was reduced comparing the exercise plus driving with the driving condition. BP and cortisol were not different among conditions. The potential of interventions, such as exercise, to counter daily stressors should be evaluated to safeguard long-term health.