Differential brain activity as a function of social evaluative stress in early adolescence: Brain function and salivary cortisol.
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ABSTRACT:
SUBMITTER: Herzberg MP
PROVIDER: S-EPMC7909600 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Stress often precedes the onset of mental health disorders and is linked to negative impacts on physical health as well. Prior research indicates that testosterone levels are related to reduced stress reactivity in some cases but correlate with increased stress responses in other cases. To resolve these inconsistencies, we tested the causal influence of testosterone on stress reactivity to a social-evaluative stressor. Further, prior work has failed to consider status-relevant individual differences such as trait dominance that may modulate the influence of testosterone on responses to stressors. Participants (n=120 males) were randomly assigned to receive exogenous testosterone or placebo (n=60 testosterone treatment group) via topical gel prior to a well-validated social-evaluative stressor. Compared to placebo, testosterone significantly increased cortisol and negative affect in response to the stressor, especially for men high in trait dominance (95% confidence intervals did not contain zero). The findings suggest that the combination of high testosterone and exposure to status-relevant social stress may confer increased risk for stress-mediated disorders, particularly for individuals high in trait dominance.
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Project description:Salivary biomarkers have been widely used to help diagnose stress, anxiety, and/or depression. This study aimed to compare the responses of three commonly investigated salivary stress biomarkers that represent the hypothalamic-pituitary-adrenal activity (cortisol; sCort) and the sympathetic activity (alpha-amylase; sAA and chromogranin A; sCgA), using academic oral presentation as a model of stress. Twenty postgraduate dental students attended the seminar class as presenter and audience. The presenters' performances were evaluated by the instructors suggesting more stress than the audience. The saliva was collected two times: before attending class and after an academic presentation (for presenters) or during the class (for audience). The pulse rates (PR) were also recorded. The results showed that the levels of all three biomarkers, as well as PR, were significantly higher in the presenter group compared with the audience group; however, the changes were most prominent with sCort and sAA (99.56 ± 12.76% for sCort, 93.48 ± 41.29% for sAA, 16.86 ± 6.42% for sCgA, and 15.06 ± 3.41% for PR). When compared between pre-post presentation, the levels of sCgA were not different, while those of sCort and sAA were significantly increased. These results suggest more sensitive reactivity to academic stress of sCort and sAA compared with sCgA and that the response of sCgA did not necessarily follow sAA pattern even though both are claimed to reflect the sympathetic activity. More studies are needed to elucidate the roles of sCgA in stress.
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Project description:Introduction:The aim of this nested study is to provide the reference intervals for already published measurements of salivary cortisol from the Croatian Adolescence Stress Study (CLASS). Material and methods:A total of 969 individuals (372 males and 597 females) were included in the reference sample (age range: 18-21 years). Salivary cortisol concentrations were determined by the enzyme immunoassay (LUCIO-Medical ELISA Salivary Cortisol Kit, Nal von Minden, Germany) in the Department of Medical Laboratory Diagnostics, University Hospital Split. Nonparametric statistics were used for calculating the reference intervals (RIs) and 90% confidence intervals (90% CIs). Results:The lower limits of RIs determined by the direct method were higher in females (> 10%) than in males for the cortisol concentrations at awakening (SCC0), 30 to 45 after awakening (SCC30-45) and at bedtime (SCCbedtime). The upper limits of RIs for the SCCbedtime were higher (> 10%) in males than in females. Females also had higher upper limits of RIs for the cortisol awakening response (CAR) and the diurnal cortisol slope (DCS) and higher lower limits of RIs for the CAR and the area under the curve with respect to ground (AUCG). The lower limits of RIs for the DCS were higher in males than in females. Conclusions:Obtained reference values open the arena for introducing salivary bioscience in Croatian clinical laboratory practice and provide important data for better understanding of gender differences in adaptation to stress during late adolescence.
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Project description:The glucocorticoid hypothesis suggests that overexposure to stress may cause permanent upregulation of cortisol. Stress in youth may therefore influence cortisol levels even in older age. Using data from the 6-Day Sample, we investigated the effects of high stress in childhood, adolescence and early adulthood - as well as individual variables contributing to these measures; parental loss, social deprivation, school and home moves, illness, divorce and job instability - upon cortisol levels at age 77 years. Waking, waking +45 min (peak) and evening salivary cortisol samples were collected from 159 participants, and the 150 who were not using steroid medications were included in this study. After correcting for multiple comparisons, the only significant association was between early-adulthood job instability and later-life peak cortisol levels. After excluding participants with dementia or possible mild cognitive impairment, early-adulthood high stress showed significant associations with lower evening and mean cortisol levels, suggesting downregulation by stress, but these results did not survive correction for multiple comparisons. Overall, our results do not provide strong evidence of a relationship between stress in youth and later-life cortisol levels, but do suggest that some more long-term stressors, such as job instability, may indeed produce lasting upregulation of cortisol, persisting into the mid-to-late seventies.
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Project description:Stressful life events increase vulnerability to problematic alcohol use, and they may do this by disrupting reward-related neural circuitry. This is particularly relevant for adolescents because alcohol use rises sharply after mid-adolescence and alcohol abuse peaks at age 20. Adolescents also report more stressors compared with children, and neural reward circuitry may be especially vulnerable to stressors during adolescence because of prefrontal cortex remodeling. Using a large sample of male participants in a longitudinal functional magnetic resonance imaging study (N = 157), we evaluated whether cumulative stressful life events between the ages of 15 and 18 were associated with reward-related brain function and problematic alcohol use at age 20 years. Higher cumulative stressful life events during adolescence were associated with decreased response in the medial prefrontal cortex (mPFC) during monetary reward anticipation and following the receipt of monetary rewards. Stress-related decreases in mPFC response during reward anticipation and following rewarding outcomes were associated with the severity of alcohol dependence. Furthermore, mPFC response mediated the association between stressful life events and later symptoms of alcohol dependence. These data are consistent with neurobiological models of addiction that propose that stressors during adolescence increase risk for problematic alcohol use by disrupting reward circuit function.
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Project description:High levels of uric acid are associated with greater risk of stress-related cardiovascular illnesses that occur disproportionately among African Americans. Whether hyperuricemia affects biological response to acute stress remains largely unknown, suggesting a need to clarify this potential connection. The current study examined how salivary uric acid (sUA) is associated with resting and reactive blood pressure - two robust predictors of hypertension and related cardiovascular disease and disparity. Healthy African Americans (N?=?107; 32% male; M age?=?31.74 years), completed the Trier Social Stress Test to induce social-evaluative stress. Systolic and diastolic blood pressure readings were recorded before, during, and after the task to assess resting and reactive change in blood pressure. Participants also provided a saliva sample at baseline that was assayed for sUA. At rest, and controlling for age, sUA was modestly associated with higher systolic (r?=?.201, p?=? .044), but not diastolic (r?=?.100, p?=? .319) blood pressure. In response to the stressor task, and once again controlling for age, sUA was also associated with higher total activation of both systolic (r?=?.219, p?=? .025) and diastolic blood pressure (r?=?.198, p?<? .044). A subsequent moderation analysis showed that associations between sUA and BP measures were significant for females, but not for males. Findings suggest that uric acid may be implicated in hypertension and cardiovascular health disparities through associations with elevated blood pressure responses to acute social stress, and that low levels of uric acid might be protective, particularly for females.
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Project description:Many neural programs that shape behavior become established during adolescence. Adverse events at this age can have enduring consequences for both adolescent and adult mental health. Here we show that repeated social stress at different stages of adolescent development differentially affects rat behavior and neuronal activity. Early-adolescent (PND 28, EA), mid-adolescent (PND 42, MA), and adult (PND 63) rats were subjected to resident-intruder social stress (7 days) and behavior was examined 24-72 h later. In EA rats selectively, resident-intruder stress increased proactive responses in the defensive burying and forced swim tests. In adult rats, resident-intruder stress decreased burying behavior regardless of whether the animal was stressed as an adult or during early adolescence. As the locus coeruleus (LC)-norepinephrine system has been implicated in proactive defense behaviors, LC neuronal activity was quantified in separate cohorts. Stressed EA rats had elevated spontaneous LC discharge rates and diminished responses to sensory stimuli compared with controls. Microinjection of a CRF antagonist into the LC selectively inhibited neurons of stressed EA rats, suggesting that EA social stress induces tonic CRF release onto LC neurons, shifting the mode of discharge to an activated state that promotes active defensive behaviors. In all adult groups, resident-intruder stress resulted in an increased phasic response to sensory stimuli with no change in spontaneous rates. MA was a transition period during which social stress did not affect behavior or LC activity. The results suggest that social stress interacts with the brain norepinephrine system to regulate defensive strategies in an age-dependent manner.
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Project description:Objective: Both lower subjective social status (SSS)-or viewing oneself as having lower status relative to others-and greater early life stress consistently relate to poorer health in adolescence. Early life stress can also negatively influence one's social relationships and may thereby shape social status. The present studies investigated how early life stress relates to the development of SSS and how SSS relates to health across the transition to college.Design: In Study 1, 91 older adolescents (Mage = 18.37) reported early life stress, society SSS, and school SSS, and they reported their society SSS and school SSS again 2 years later. In Study 2, 94 first-year college students (Mage = 18.20) reported early life stress and society SSS at study entry and reported their dorm SSS, university SSS, and mental health monthly throughout the year.Results: Greater early life stress was related to lower society SSS, but not school SSS, in both studies. In Study 2, dorm and university SSS and early life stress were uniquely related to mental health, although associations weakened over time.Conclusion: Early life stress may predispose people to have low society SSS, and both low school SSS and high early life stress may increase risk for poorer health during transition periods.
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Project description:Early-life adversity has been associated with a life-long increased risk for psychopathology and chronic health problems. These long-term negative effects have been explained through stress sensitization, which may involve dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis through either increased or decreased reactivity. The present meta-analysis assessed for the first time the effect of early-life adversity on cortisol response to social stress. Thirty data sets were included in the meta-analysis, in which early-life adversity and salivary cortisol response to social stress were assessed in 4292 individuals of different ages. Results indicated a moderate effect size (g?=?-0.39) in overall cortisol levels across studies. Separate analyses of cortisol at different stages of response showed large effect sizes at peak and recovery, and a moderate effect at baseline. Heterogeneity was large in this sample of studies and several moderators were identified. The effect size was larger in studies that focused on maltreatment compared to those that included other adversities, and in adults compared to children and adolescents. Percent of women in each sample and methodological quality were positive predictors of the effect size. Publication bias may be present, but the analysis was hampered by the high heterogeneity. Therefore, these results support the association between early-life adversity and blunted cortisol response to social stress, and they suggest that the long-term negative effects of early-life adversity may reach maximum levels in adults.
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Project description:Background: Posttraumatic stress disorder (PTSD) is associated with dysregulated neural, cortisol, and cardiac stress reactivity and recovery. This understanding is predominantly based on studies in adults applying emotional-cognitive and trauma-related stimuli inducing negative emotions or perceived threat. Despite large numbers of adolescents with PTSD, few studies are available on neurobiological stress reactivity in this population. Moreover, no previous studies investigated neural reactivity to social-evaluative stress. Objective: To investigate functional brain connectivity, cortisol and cardiac reactivity to acute social-evaluative stress, and additional cortisol measures in trauma-exposed adolescents with and without high PTSD symptoms. Method: A speech preparation task to induce acute social-evaluative stress elicited by anticipatory threat, was used in a subsample of the Amsterdam Born Child and their Development (ABCD) birth cohort, consisting of trauma-exposed adolescents with (n = 20) and without (n = 29) high PTSD symptoms. Psychophysiological interaction analyses were performed to assess group differences in functional connectivity of the hippocampus, mPFC and amygdala during social-evaluative stress and recovery, measured by fMRI. Additionally, perceived stress, heart rate and cortisol stress reactivity and recovery, cortisol awakening response and day curve were compared. Results: The stressor evoked significant changes in heart rate and perceived stress, but not cortisol. The PTSD symptom and control groups differed in functional connectivity between the hippocampus and cerebellum, middle and inferior frontal gyrus, and the mPFC and inferior frontal gyrus during social-evaluative stress versus baseline. Mostly, the same patterns were found during recovery versus baseline. We observed no significant group differences in amygdala connectivity, and cortisol and cardiac measures. Conclusions: Our findings suggest threat processing in response to social-evaluative stress is disrupted in adolescents with PTSD symptoms. Our findings are mainly but not entirely in line with findings in adults with PTSD, which denotes the importance to investigate adolescents with PTSD as a separate population.
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