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Douglas A Granger - One of the best experts on this subject based on the ideXlab platform.
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Prenatal Drug Exposure and Adolescent Cortisol Reactivity: Association with Behavioral Concerns.
Journal of Developmental and Behavioral Pediatrics, 2016Co-Authors: Stacy Buckingham-howes, Douglas A Granger, Dayna Mazza, Yan Wang, Maureen M. BlackAbstract:Objective: To examine stress Reactivity in a sample of adolescents with prenatal drug exposure (PDE) by examining the consequences of PDE on stress-related adrenocortical Reactivity, behavioral problems, and drug experimentation during adolescence. Methods: Participants (76 PDE, 61 non-drug exposed [NE]; 99% African-American; 50% male; mean age = 14.17 yr, SD = 1.17) provided a urine sample, completed a drug use questionnaire, and provided saliva samples (later assayed for Cortisol) before and after a mild laboratory stress task. Caregivers completed the Behavior Assessment System for Children, Second Edition (BASC II) and reported their relationship to the adolescent. Results: The NE group was more likely to exhibit task-related Cortisol Reactivity compared to the PDE group. Overall behavior problems and drug experimentation were comparable across groups with no differences between PDE and NE groups. In unadjusted mediation analyses, Cortisol Reactivity mediated the association between PDE and BASC II aggression scores (95% bootstrap confidence interval [CI], 0.04–4.28), externalizing problems scores (95% bootstrap CI, 0.03–4.50), and drug experimentation (95% bootstrap CI, 0.001–0.54). The associations remain with the inclusion of gender as a covariate but not when age is included. Conclusion: Findings support and expand current research in Cortisol Reactivity and PDE by demonstrating that Cortisol Reactivity attenuates the association between PDE and behavioral problems (aggression) and drug experimentation. If replicated, PDE may have long-lasting effects on stress-sensitive physiological mechanisms associated with behavioral problems (aggression) and drug experimentation in adolescence.
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sleep problems predict Cortisol Reactivity to stress in urban adolescents
Physiology & Behavior, 2016Co-Authors: Sylvie Mrug, Douglas A Granger, Bulent Turan, Anna TysonAbstract:This study examined the role of sleep problems and sleep duration on stress-related HPA axis Reactivity among urban, low income adolescents. A total of 84 adolescents (M age 13.36 years; 50% male; 95% African American) and their parents provided information on adolescents' sleep problems and sleep quantity. Adolescents completed a standardized social stress test in the laboratory (the Trier Social Stress Test; TSST). Saliva samples collected before and after the TSST yielded measures of Cortisol pre-test, 15 min post-test, and 55 min post-test, as well as overall Cortisol secretion and its increase (AUCG and AUCI). More sleep problems and longer sleep duration predicted higher Cortisol Reactivity to the TSST, particularly among females. Self-reports of sleep were more consistently related to stress-related Cortisol Reactivity than parent reports. Sleep problems and longer sleep duration may place adolescents at risk for HPA axis hyper-Reactivity to stress, contributing to academic, behavioral and health problems.
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digit ratio 2d 4d moderates the relationship between Cortisol Reactivity and self reported externalizing behavior in young adolescent males
Biological Psychology, 2015Co-Authors: Jill Portnoy, Adrian Raine, Andrea L Glenn, Frances R Chen, Olivia Choy, Douglas A GrangerAbstract:Abstract Although reduced Cortisol Reactivity to stress and increased circulating testosterone level are hypothesized to be associated with higher levels of externalizing behavior, empirical findings are inconsistent. One factor that may account for the heterogeneity in these relationships is prenatal testosterone exposure. This study examined whether the second-to-fourth digit ratio (2D:4D), a putative marker of prenatal testosterone exposure, moderates the relationships of testosterone and Cortisol Reactivity with externalizing behavior. Left and right hand 2D:4D and self-reported externalizing behavior were measured in a sample of 353 young adolescents ( M age = 11.92 years; 178 females; 79.7% African American). Saliva samples were collected before and after a stress task and later assayed for Cortisol. Testosterone levels were determined from an AM saliva sample. 2D:4D interacted with Cortisol Reactivity to predict externalizing behavior in males, but not females. In males, low Cortisol Reactivity was associated with higher levels of aggression and rule-breaking behavior, but only among subjects with low 2D:4D (i.e., high prenatal testosterone). Findings suggest the importance of a multi-systems approach in which interactions between multiple hormones are taken into account. Furthermore, results demonstrate the importance of considering the organizational influence of prenatal testosterone in order to understand the activational influence of circulating hormones during adolescence.
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Prenatal Cocaine Exposure and Infant Cortisol Reactivity
Child Development, 2009Co-Authors: Rina D Eiden, Yvette Veira, Douglas A GrangerAbstract:This study examined the effects of prenatal cocaine exposure on infant hypothalamic-pituitary-adrenal axis activity and Reactivity at 7 months of infant age. Participants were 168 caregiver-infant dyads (87 cocaine exposed, 81 not cocaine exposed; 47% boys). Maternal behavior, caregiving instability, and infant growth and behavior were assessed, and children's saliva was sampled before, during, and after standardized procedures designed to elicit emotional arousal. Results revealed cocaine-exposed infants had a high amplitude trajectory of Cortisol Reactivity compared to non-cocaine-exposed infants. Infant gender and caregiving instability moderated this association. The findings support a dual hazard vulnerability model and have implications for evolutionary-developmental theories of individual differences in biological sensitivity to context.
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the association between prenatal exposure to cigarettes and Cortisol Reactivity and regulation in 7 month old infants
Developmental Psychobiology, 2008Co-Authors: Pamela Schuetze, Francisco A Lopez, Douglas A Granger, Rina D EidenAbstract:We examined the association between prenatal exposure to cigarettes and adrenocortical responses to stress in 7-month old infants. Cortisol levels were assessed twice prior to and twice following affect-eliciting procedures in 111 (59 exposed and 52 nonexposed) infants. Cortisol Reactivity was defined as the difference between the peak poststressor cortical level and the pretask Cortisol level. Higher values indicated higher Cortisol Reactivity. Exposed infants had higher peak Cortisol Reactivity than non exposed infants. There were no differences in pretask Cortisol levels. Maternal hostility mediated the association between cigarette exposure and peak Cortisol Reactivity. Furthermore, infant gender moderated this association such that exposed boys had significantly higher peak Cortisol Reactivity than nonexposed infants or exposed girls. These findings provide additional evidence that prenatal cigarette exposure is associated with dysregulation during infancy and that early adverse, non-social experiences may have relatively long-lasting effects on Cortisol Reactivity in infants.
Katja Petrowski - One of the best experts on this subject based on the ideXlab platform.
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High/low Cortisol Reactivity and food intake in people with obesity and healthy weight
Translational Psychiatry, 2020Co-Authors: Benedict Herhaus, Enrico Ullmann, George Chrousos, Katja PetrowskiAbstract:Increased food intake, termed “comfort eating”, is a pathologic coping mechanism in chronic stress. Cortisol Reactivity under stress is a potent predictor of stress-induced eating behavior affecting the body mass index (BMI). However, Cortisol Reactivity and food intake under stress in people with obesity has not been evaluated. The aim of this study was to investigate the effect of high/low Cortisol Reactivity on food intake in people with obesity and healthy weight test controls, following standardized stress induction and a resting condition. Thirty-six men and women with obesity (BMI: 33.00 ± 3.23 kg/m²), as well as 36 age- and gender-matched healthy weight controls (BMI: 21.98 ± 1.81 kg/m²) were categorized into high Cortisol reactors (HCR) and low Cortisol reactors (LCR) in the Trier Social Stress Test (TSST). Following the TSST and a resting condition, the food intake of all participants was recorded in a standardized laboratory meal. Obese HCR demonstrated a significantly higher food intake than LCR ( t (34) = −2.046, p ≤ 0.05). However, there were no significant differences between HCR and LCR in the healthy weight controls ( p = 0.26). In addition, HCR of the people with obesity showed lower values in the emotion coping strategy of cognitive reappraisal than obese LCR ( t (32) = 2.087, p ≤ 0.05). In conclusion, the magnitude of the Cortisol Reactivity to stress predicts stress-induced food intake in people with obesity, but not in the healthy weight controls. Limited use of cognitive reappraisal in emotion regulation in the obese HCR may be a marker of vulnerability to stress-induced eating.
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high low Cortisol Reactivity and food intake in people with obesity and healthy weight
Translational Psychiatry, 2020Co-Authors: Benedict Herhaus, George P. Chrousos, Enrico Ullmann, Katja PetrowskiAbstract:Increased food intake, termed “comfort eating”, is a pathologic coping mechanism in chronic stress. Cortisol Reactivity under stress is a potent predictor of stress-induced eating behavior affecting the body mass index (BMI). However, Cortisol Reactivity and food intake under stress in people with obesity has not been evaluated. The aim of this study was to investigate the effect of high/low Cortisol Reactivity on food intake in people with obesity and healthy weight test controls, following standardized stress induction and a resting condition. Thirty-six men and women with obesity (BMI: 33.00 ± 3.23 kg/m²), as well as 36 age- and gender-matched healthy weight controls (BMI: 21.98 ± 1.81 kg/m²) were categorized into high Cortisol reactors (HCR) and low Cortisol reactors (LCR) in the Trier Social Stress Test (TSST). Following the TSST and a resting condition, the food intake of all participants was recorded in a standardized laboratory meal. Obese HCR demonstrated a significantly higher food intake than LCR (t (34) = −2.046, p ≤ 0.05). However, there were no significant differences between HCR and LCR in the healthy weight controls (p = 0.26). In addition, HCR of the people with obesity showed lower values in the emotion coping strategy of cognitive reappraisal than obese LCR (t (32) = 2.087, p ≤ 0.05). In conclusion, the magnitude of the Cortisol Reactivity to stress predicts stress-induced food intake in people with obesity, but not in the healthy weight controls. Limited use of cognitive reappraisal in emotion regulation in the obese HCR may be a marker of vulnerability to stress-induced eating.
Enrico Ullmann - One of the best experts on this subject based on the ideXlab platform.
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High/low Cortisol Reactivity and food intake in people with obesity and healthy weight
Translational Psychiatry, 2020Co-Authors: Benedict Herhaus, Enrico Ullmann, George Chrousos, Katja PetrowskiAbstract:Increased food intake, termed “comfort eating”, is a pathologic coping mechanism in chronic stress. Cortisol Reactivity under stress is a potent predictor of stress-induced eating behavior affecting the body mass index (BMI). However, Cortisol Reactivity and food intake under stress in people with obesity has not been evaluated. The aim of this study was to investigate the effect of high/low Cortisol Reactivity on food intake in people with obesity and healthy weight test controls, following standardized stress induction and a resting condition. Thirty-six men and women with obesity (BMI: 33.00 ± 3.23 kg/m²), as well as 36 age- and gender-matched healthy weight controls (BMI: 21.98 ± 1.81 kg/m²) were categorized into high Cortisol reactors (HCR) and low Cortisol reactors (LCR) in the Trier Social Stress Test (TSST). Following the TSST and a resting condition, the food intake of all participants was recorded in a standardized laboratory meal. Obese HCR demonstrated a significantly higher food intake than LCR ( t (34) = −2.046, p ≤ 0.05). However, there were no significant differences between HCR and LCR in the healthy weight controls ( p = 0.26). In addition, HCR of the people with obesity showed lower values in the emotion coping strategy of cognitive reappraisal than obese LCR ( t (32) = 2.087, p ≤ 0.05). In conclusion, the magnitude of the Cortisol Reactivity to stress predicts stress-induced food intake in people with obesity, but not in the healthy weight controls. Limited use of cognitive reappraisal in emotion regulation in the obese HCR may be a marker of vulnerability to stress-induced eating.
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high low Cortisol Reactivity and food intake in people with obesity and healthy weight
Translational Psychiatry, 2020Co-Authors: Benedict Herhaus, George P. Chrousos, Enrico Ullmann, Katja PetrowskiAbstract:Increased food intake, termed “comfort eating”, is a pathologic coping mechanism in chronic stress. Cortisol Reactivity under stress is a potent predictor of stress-induced eating behavior affecting the body mass index (BMI). However, Cortisol Reactivity and food intake under stress in people with obesity has not been evaluated. The aim of this study was to investigate the effect of high/low Cortisol Reactivity on food intake in people with obesity and healthy weight test controls, following standardized stress induction and a resting condition. Thirty-six men and women with obesity (BMI: 33.00 ± 3.23 kg/m²), as well as 36 age- and gender-matched healthy weight controls (BMI: 21.98 ± 1.81 kg/m²) were categorized into high Cortisol reactors (HCR) and low Cortisol reactors (LCR) in the Trier Social Stress Test (TSST). Following the TSST and a resting condition, the food intake of all participants was recorded in a standardized laboratory meal. Obese HCR demonstrated a significantly higher food intake than LCR (t (34) = −2.046, p ≤ 0.05). However, there were no significant differences between HCR and LCR in the healthy weight controls (p = 0.26). In addition, HCR of the people with obesity showed lower values in the emotion coping strategy of cognitive reappraisal than obese LCR (t (32) = 2.087, p ≤ 0.05). In conclusion, the magnitude of the Cortisol Reactivity to stress predicts stress-induced food intake in people with obesity, but not in the healthy weight controls. Limited use of cognitive reappraisal in emotion regulation in the obese HCR may be a marker of vulnerability to stress-induced eating.
Elissa S Epel - One of the best experts on this subject based on the ideXlab platform.
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good stress bad stress and oxidative stress insights from anticipatory Cortisol Reactivity
Psychoneuroendocrinology, 2013Co-Authors: Kirstin Aschbacher, Aoife Odonovan, Owen M Wolkowitz, Firdaus S Dhabhar, Yali Su, Elissa S EpelAbstract:Chronic psychological stress appears to accelerate biological aging, and oxidative damage is an important potential mediator of this process. However, the mechanisms by which psychological stress promotes oxidative damage are poorly understood. This study investigates the theory that Cortisol increases in response to an acutely stressful event have the potential to either enhance or undermine psychobiological resilience to oxidative damage, depending on the body's prior exposure to chronic psychological stress. In order to achieve a range of chronic stress exposure, forty-eight post-menopausal women were recruited in a case-control design that matched women caring for spouses with dementia (a chronic stress model) with similarly aged control women whose spouses were healthy. Participants completed a questionnaire assessing perceived stress over the previous month and provided fasting blood. Three markers of oxidative damage were assessed: 8-iso-prostaglandin F2α (IsoP), lipid peroxidation, 8-hydroxyguanosine (8-oxoG) and 8-hydroxy-2′-deoxyguanosine (8-OHdG), reflecting oxidative damage to RNA/DNA respectively. Within approximately one week, participants completed a standardized acute laboratory stress task while salivary Cortisol responses were measured. The increase from 0 to 30 min was defined as “peak” Cortisol Reactivity, while the increase from 0 to 15 min was defined as “anticipatory” Cortisol Reactivity, representing a Cortisol response that began while preparing for the stress task. Women under chronic stress had higher 8-oxoG, oxidative damage to RNA (p < .01). A moderated mediation model was tested, in which it was hypothesized that heightened anticipatory Cortisol Reactivity would mediate the relationship between perceived stress and elevated oxidative stress damage, but only among women under chronic stress. Consistent with this model, bootstrapped path analysis found significant indirect paths from perceived stress to 8-oxoG and IsoP (but not 8-OHdG) via anticipatory Cortisol Reactivity, showing the expected relations among chronically stressed participants (p ≤ .01) Intriguingly, among those with low chronic stress exposure, moderate (compared to low) levels of perceived stress were associated with reduced levels of oxidative damage. Hence, this study supports the emerging model that chronic stress exposure promotes oxidative damage through frequent and sustained activation of the hypothalamic-pituitary-adrenal axis. It also supports the less studied model of ‘eustress’ – that manageable levels of life stress may enhance psychobiological resilience to oxidative damage.
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Good stress, bad stress and oxidative stress: Insights from anticipatory Cortisol Reactivity
Psychoneuroendocrinology, 2013Co-Authors: Kirstin Aschbacher, Owen M Wolkowitz, Firdaus S Dhabhar, Yali Su, Aoife O'donovan, Elissa S EpelAbstract:Chronic psychological stress appears to accelerate biological aging, and oxidative damage is an important potential mediator of this process. However, the mechanisms by which psychological stress promotes oxidative damage are poorly understood. This study investigates the theory that Cortisol increases in response to an acutely stressful event have the potential to either enhance or undermine psychobiological resilience to oxidative damage, depending on the body's prior exposure to chronic psychological stress. In order to achieve a range of chronic stress exposure, forty-eight post-menopausal women were recruited in a case-control design that matched women caring for spouses with dementia (a chronic stress model) with similarly aged control women whose spouses were healthy. Participants completed a questionnaire assessing perceived stress over the previous month and provided fasting blood. Three markers of oxidative damage were assessed: 8-iso-prostaglandin F2α (IsoP), lipid peroxidation, 8-hydroxyguanosine (8-oxoG) and 8-hydroxy-2′-deoxyguanosine (8-OHdG), reflecting oxidative damage to RNA/DNA respectively. Within approximately one week, participants completed a standardized acute laboratory stress task while salivary Cortisol responses were measured. The increase from 0 to 30 min was defined as “peak” Cortisol Reactivity, while the increase from 0 to 15 min was defined as “anticipatory” Cortisol Reactivity, representing a Cortisol response that began while preparing for the stress task. Women under chronic stress had higher 8-oxoG, oxidative damage to RNA (p
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physical activity moderates effects of stressor induced rumination on Cortisol Reactivity
Psychosomatic Medicine, 2011Co-Authors: Eli Puterman, Aoife Odonovan, Owen M Wolkowitz, Nancy E Adler, A Tomiyama, Margaret E Kemeny, Elissa S EpelAbstract:Objective: Physically active individuals have lower rates of morbidity and mortality, and recent evidence indicates that physical activity may be particularly beneficial to those experiencing chronic stress. The tendency to ruminate increases and prolongs physiological stress responses, including hypothalamic-pituitary-adrenal (HPA) axis responses as indexed by Cortisol Reactivity to stressful experiences. We examined the association between ruminating in response to a laboratory stressor task and HPA axis Reactivity and recovery and examined whether a physically active life-style moderates the associations between rumination and Cortisol output trajectories. Methods: Forty-six postmenopausal women underwent the Trier Social Stress Test, whereas salivary Cortisol was repeatedly measured. Twenty-five minutes after the end of the stressor, participants reported level of rumination in response to the stress. Results: Findings indicate that physical activity moderated the initial rate (B =-0.10, standard error = 0.04, p < .05) and curvature (B =-0.03, standard error = 0.01, p = .06) of the relationship between rumination and log-transformed Cortisol trajectory. Among sedentary participants, those who responded to the stressor with higher levels of rumination had a more rapid initial increase in Cortisol level (0.26 versus 0.21, p < .001), a later peak in Cortisol Reactivity (56 versus 39 minutes), and a delayed recovery from stress (curvature:-0.07 versus-0.08, p < .001) compared with those with lower levels of rumination. In active participants, Cortisol trajectories were equivalent, regardless of the level of rumination. Conclusions: In sum, individuals who maintain a physically active life-style may be protected against the effects of rumination on HPA axis Reactivity to and recovery from acute stress. © 2011 by the American Psychosomatic Society.
Benedict Herhaus - One of the best experts on this subject based on the ideXlab platform.
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High/low Cortisol Reactivity and food intake in people with obesity and healthy weight
Translational Psychiatry, 2020Co-Authors: Benedict Herhaus, Enrico Ullmann, George Chrousos, Katja PetrowskiAbstract:Increased food intake, termed “comfort eating”, is a pathologic coping mechanism in chronic stress. Cortisol Reactivity under stress is a potent predictor of stress-induced eating behavior affecting the body mass index (BMI). However, Cortisol Reactivity and food intake under stress in people with obesity has not been evaluated. The aim of this study was to investigate the effect of high/low Cortisol Reactivity on food intake in people with obesity and healthy weight test controls, following standardized stress induction and a resting condition. Thirty-six men and women with obesity (BMI: 33.00 ± 3.23 kg/m²), as well as 36 age- and gender-matched healthy weight controls (BMI: 21.98 ± 1.81 kg/m²) were categorized into high Cortisol reactors (HCR) and low Cortisol reactors (LCR) in the Trier Social Stress Test (TSST). Following the TSST and a resting condition, the food intake of all participants was recorded in a standardized laboratory meal. Obese HCR demonstrated a significantly higher food intake than LCR ( t (34) = −2.046, p ≤ 0.05). However, there were no significant differences between HCR and LCR in the healthy weight controls ( p = 0.26). In addition, HCR of the people with obesity showed lower values in the emotion coping strategy of cognitive reappraisal than obese LCR ( t (32) = 2.087, p ≤ 0.05). In conclusion, the magnitude of the Cortisol Reactivity to stress predicts stress-induced food intake in people with obesity, but not in the healthy weight controls. Limited use of cognitive reappraisal in emotion regulation in the obese HCR may be a marker of vulnerability to stress-induced eating.
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high low Cortisol Reactivity and food intake in people with obesity and healthy weight
Translational Psychiatry, 2020Co-Authors: Benedict Herhaus, George P. Chrousos, Enrico Ullmann, Katja PetrowskiAbstract:Increased food intake, termed “comfort eating”, is a pathologic coping mechanism in chronic stress. Cortisol Reactivity under stress is a potent predictor of stress-induced eating behavior affecting the body mass index (BMI). However, Cortisol Reactivity and food intake under stress in people with obesity has not been evaluated. The aim of this study was to investigate the effect of high/low Cortisol Reactivity on food intake in people with obesity and healthy weight test controls, following standardized stress induction and a resting condition. Thirty-six men and women with obesity (BMI: 33.00 ± 3.23 kg/m²), as well as 36 age- and gender-matched healthy weight controls (BMI: 21.98 ± 1.81 kg/m²) were categorized into high Cortisol reactors (HCR) and low Cortisol reactors (LCR) in the Trier Social Stress Test (TSST). Following the TSST and a resting condition, the food intake of all participants was recorded in a standardized laboratory meal. Obese HCR demonstrated a significantly higher food intake than LCR (t (34) = −2.046, p ≤ 0.05). However, there were no significant differences between HCR and LCR in the healthy weight controls (p = 0.26). In addition, HCR of the people with obesity showed lower values in the emotion coping strategy of cognitive reappraisal than obese LCR (t (32) = 2.087, p ≤ 0.05). In conclusion, the magnitude of the Cortisol Reactivity to stress predicts stress-induced food intake in people with obesity, but not in the healthy weight controls. Limited use of cognitive reappraisal in emotion regulation in the obese HCR may be a marker of vulnerability to stress-induced eating.
