Cortisol stress reactivity to the trier social stress test in obese adults

Approximately 600 million adults worldwide suffer from obesity. In addition to individual’s eating behavior and lack of physical activity in the development of obesity and overweight, psychosocial stress as well as hormonal stress reactivity must also be considered as important contributing factors. In the current study we compared the cortisol stress response pathway in a psychosocial stress induction (Trier Social Stress Test; TSST) with obese individuals and normal-weight controls. 32 obese individuals (17 females; mean age = 33.94 years, SD = 11.31 years) and 32 normal-weight controls (17 females; mean age = 29.09 years, SD = 10.46 years) underwent the TSST. The salivary cortisol responses and three appraisal questionnaires (Primary Appraisal Secondary Appraisal, Visual Analogue Scale, Trier Inventory for Chronic Stress) were measured. After stress induction, there was a significant main group difference between the obese individuals and the normal-weight controls for cortisol, with lower baseline and post-stress cortisol levels in the obese individuals. Nevertheless, the obese individuals as well as the normal-weight controls showed no significant difference in the self reported assessment of the stress condition but some significant differences in the cognitive appraisal of the TSST. In conclusion, the induction of psychosocial stress showed differences in the cortisol patterns between the obese individuals and the normal-weight controls. Furthermore, the present data suggest that obesity leads to lower cortisol activity, which may indicate alterations in the Hypothalamic-pituitary-adrencortical (HPA) axis

Cortisol Stress Reactivity to the Trier Social Stress Test in Obese Adults

Objective: Approximately 600 million adults worldwide suffer from obesity. In addition to individual’s eating behavior and lack of physical activity in the development of obesity and overweight, psychosocial stress as well as hormonal stress reactivity must also be considered as important contributing factors. In the current study we compared the cortisol stress response pathway in a psychosocial stress induction (Trier Social Stress Test; TSST) with obese individuals and normal-weight controls. Method: 32 obese individuals (17 females; mean age = 33.94 years, SD = 11.31 years) and 32 normal-weight controls (17 females; mean age = 29.09 years, SD = 10.46 years) underwent the TSST. The salivary cortisol responses and three appraisal questionnaires (Primary Appraisal Secondary Appraisal, Visual Analogue Scale, Trier Inventory for Chronic Stress) were measured. Results: After stress induction, there was a significant main group difference between the obese individuals and the normal-weight controls for cortisol, with lower baseline and post-stress cortisol levels in the obese individuals. Nevertheless, the obese individuals as well as the normal-weight controls showed no significant difference in the self-reported assessment of the stress condition but some significant differences in the cognitive appraisal of the TSST. Conclusion: In conclusion, the induction of psychosocial stress showed differences in the cortisol patterns between the obese individuals and the normal-weight controls. Furthermore, the present data suggest that obesity leads to lower cortisol activity, which may indicate alterations in the Hypothalamic-pituitary-adrencortical (HPA) axis

High/low cortisol reactivity and food intake in people with obesity and healthy weight

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

Hormonal responsiveness in the Trier Social Stress Test and the dexamethasone-corticotropin releasing hormone test in healthy individuals

A number of different laboratory procedures investigate the hormonal response in a standardized pharmacological challenge test (dexamethasone-corticotropin releasing hormone; DEX-CRH) or in a psychosocial stress induction on the hypothalamic-pituitary-adrenocortical axis by the Trier Social Stress Test (TSST). However, the magnitude of the response related to the different stressors and the interaction of the responsiveness between the two tests is still unclear. Fifty-two participants underwent both the DEX-CRH test and the TSST on two separate days. The cortisol and the plasma adrenocorticotropic hormone (ACTH) release were assessed before and after the stress tests. For a specification of the cortisol response to both conditions, subgroups of high- and low-cortisol responders to the TSST and the DEX-CRH test were formed. The healthy participants showed a substantial increase in the ACTH and the cortisol concentration after the two tests. This increase was 3 times greater in the TSST than the DEX-CRH test. High responders in both tests demonstrated a higher factor of the cortisol reactivity ratio (TSST/DEX-CRH test). Psychosocial stress as induced by the TSST was associated with a significantly greater increase in cortisol compared to the DEX-CRH test, even though the ACTH response displayed no differences. Our findings indicate an interaction of the hormonal responsiveness between the two tests with regard to the cortisol patterns

Mobile Heart Rate Variability Biofeedback Improves Autonomic Activation and Subjective Sleep Quality of Healthy Adults - A Pilot Study

Objective: Restorative sleep is associated with increased autonomous parasympathetic nervous system activity that might be improved by heart rate variability-biofeedback (HRV-BF) training. Hence the aim of this study was to investigate the effect of a four-week mobile HRV-BF intervention on the sleep quality and HRV of healthy adults. - Methods: In a prospective study, 26 healthy participants (11 females; mean age: 26.04 ± 4.52 years; mean body mass index: 23.76 ± 3.91 kg/m²) performed mobile HRV-BF training with 0.1 Hz breathing over four weeks, while sleep quality, actigraphy and HRV were measured before and after the intervention. - Results: Mobile HRV-BF training with 0.1 Hz breathing improved the subjective sleep quality in healthy adults [t(24) = 4.9127, p ≤ 0.001, d = 0.99] as measured by the Pittsburgh Sleep Quality Index. In addition, mobile HRV-BF training with 0.1 Hz breathing was associated with an increase in the time and frequency domain parameters SDNN, Total Power and LF after four weeks of intervention. No effect was found on actigraphy metrics. - Conclusions: Mobile HRV-BF intervention with 0.1 Hz breathing increased the reported subjective sleep quality and may enhance the vagal activity in healthy young adults. HRV-BF training emerges as a promising tool for improving sleep quality and sleep-related symptom severity by means of normalizing an impaired autonomic imbalance during sleep

Kinetics of plasma cell-free DNA under a highly standardized and controlled stress induction

Psychological stress affects the immune system and activates peripheral inflammatory pathways. Circulating cell-free DNA (cfDNA) is associated with systemic inflammation, and recent research indicates that cfDNA is an inflammatory marker that is sensitive to psychological stress in humans. The present study investigated the effects of acute stress on the kinetics of cfDNA in a within-subjects design. Twenty-nine males (mean age: 24.34 ± 4.08 years) underwent both the Trier Social Stress Test (TSST) and a resting condition. Blood samples were collected at two time points before and at 9 time points up to 105 min after both conditions. The cfDNA immediately increased 2-fold after the TSST and returned to baseline levels after 30 min after the test, showing that a brief psychological stressor was sufficient to evoke a robust and rapid increase in cfDNA levels. No associations were detected between perceived stress, whereas subjects with higher basal cfDNA levels showed higher increases. The rapid cfDNA regulation might be attributed to the transient activation of immune cells caused by neuroendocrine-immune activation. Further research is required to evaluate the reliability of cfDNA as a marker of neuroendocrine-immune activation, which could be used for diagnostics purposes or monitoring of treatment progression

Kinetics of Plasma Cell-Free DNA under a Highly Standardized and Controlled Stress Induction

Psychological stress affects the immune system and activates peripheral inflammatory pathways. Circulating cell-free DNA (cfDNA) is associated with systemic inflammation, and recent research indicates that cfDNA is an inflammatory marker that is sensitive to psychological stress in humans. The present study investigated the effects of acute stress on the kinetics of cfDNA in a within-subjects design. Twenty-nine males (mean age: 24.34 ± 4.08 years) underwent both the Trier Social Stress Test (TSST) and a resting condition. Blood samples were collected at two time points before and at 9 time points up to 105 min after both conditions. The cfDNA immediately increased 2-fold after the TSST and returned to baseline levels after 30 min after the test, showing that a brief psychological stressor was sufficient to evoke a robust and rapid increase in cfDNA levels. No associations were detected between perceived stress, whereas subjects with higher basal cfDNA levels showed higher increases. The rapid cfDNA regulation might be attributed to the transient activation of immune cells caused by neuroendocrine-immune activation. Further research is required to evaluate the reliability of cfDNA as a marker of neuroendocrine-immune activation, which could be used for diagnostics purposes or monitoring of treatment progression

Cortisol reactivity in patients with anorexia nervosa after stress induction

There is a need of experimental studies on biomarkers in patients with anorexia nervosa (P-AN), especially in the context of stress, in order to foster understanding in illness maintenance. To this end, the cortisol response to an acute stressor was investigated in n=26 P(-AN) (BMI: 19.3 ± 3.4kg/m(2)), age, and gender matched to n=26 healthy controls (HC; BMI: 23.08 ± 3.3kg/m(2)). For this purpose, salivary cortisol parameters were assessed in two experimental conditions: (1) rest/no intervention and (2) stress intervention (TSST; Trier Social Stress Test). In addition, psychological indicators of stress were assessed (Primary Appraisal Secondary Appraisal, Visual Analogue Scale, and Trier Inventory for the assessment of Chronic Stress), as well as psychological distress, depression, and eating disorder (ED) symptoms. A 2x2x8 ANOVA demonstrated elevated cortisol levels in P-AN in the resting condition. In the stress intervention no significant group effect in terms of cortisol (F (1, 50)=0.69; p=0.410; eta p2=0.014). A significant condition (F (1, 50)=20.50; p=0.000; eta p2=0.291) and time effect (F(2.71, 135.44)=11.27; p=0.000; eta p2=0.20) were revealed, as well as two significant interaction effects. First: Condition x group (F (1, 50)=4.17, p=0.046; eta p2=0.077) and second: Condition x time (F (2.71, 135.44)=16.07, p=0.000, eta p2=0.24.). In terms of AUC(G), no significant differences between both groups were exhibited. Regardless, significant results were evinced in terms of an increase (AUC(i): F(1, 50)=20.66, p=0.015, eta p2=0.113), baseline to peak (+20min post-TSST: t(5)=16.51 (9.02), p=0.029) and reactivity (M-PAN=0.73 vs. M-HC=4.25, p=0.036). In addition, a significant correlation between AUC(G) and BMI: r (24)=-0.42, p=0.027 was demonstrated, but not between AUC(i) and BMI (r (24)=-0.26, p=0.20). Psychological indices suggested higher levels of chronic and perceived stress in P-AN relative to HC. However, stress perception in the stress condition (VAS) was comparable. Additional analyses demonstrated that ED-symptoms are highly correlated with psychological distress and depression, but not with BMI. In addition, it could be demonstrated that reactivity is rather related to ED-symptoms and psychological burden than to BMI. In conclusion, P-AN showed elevated basal cortisol levels at rest and exhibited a blunted cortisol reactivity to the TSST as evinced by salivary cortisol parameters. Further, it was shown that weight recovery influences reversibility of hypercortisolemia, i.e., cortisol levels normalize with weight gain. However, HPAA (hypothalamus-pituitary-adrenal axis) irregularities in terms of reactivity persist even at a BMI <= 19.3 (+/- 3.4). Our data suggest that pronounced psychological burden in P-AN, have a greater impact on the HPAA functionality (secondary to the ED) than BMI itself