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.

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.

The neurotrophic protein brain-derived neurotrophic factor (BDNF) plays a pivotal role in brain function and is affected by acute and chronic stress. We here investigate the patterns of BDNF and cortisol stress reactivity and recovery under the standardized stress protocol of the TSST and the effect of perceived chronic stress on the basal BDNF levels in healthy young men. Twenty-nine lean young men underwent the Trier Social Stress Test (TSST) and a resting condition. Serum BDNF and cortisol were measured before and repeatedly after both conditions. The perception of chronic stress was assessed by the Trier Inventory for Chronic Stress (TICS). After the TSST, there was a significant increase over time for BDNF and cortisol. Stronger increase in cortisol in response to stress was linked to an accelerated BDNF decline after stress. Basal resting levels of BDNF was significantly predicted by chronic stress perception. The increased BDNF level following psychosocial stress suggest a stress-induced neuroprotective mechanism. The presumed interplay between BDNF and the HPA-axis indicates an antagonistic relationship of cortisol on BDNF recovery post-stress. Chronically elevated high cortisol levels, as present in chronic stress, could thereby contribute to reduced neurogenesis, and an increased risk of neurodegenerative conditions in persons suffering from chronic stress.

Objective: Some individuals with panic disorder (PD) display reduced heart rate variability (HRV), which may result in an increased risk of cardiovascular mortality. Heart rate variability–biofeedback (HRV-BF) training has been shown to improve the modulation of the autonomic activity. Therefore, this randomized controlled trial was conducted to investigate the effect of a 4-week HRV-BF intervention in individuals with PD. HRV-BF training improved the modulation of the autonomic activity. Therefore, with this randomized controlled trial, we aimed to investigate the effect of a 4-week HRV-BF intervention in people with PD. Methods: Thirty-six women and 16 men with PD (mean age = 35.85 [15.60] years) were randomly allocated either to HRV-BF with 0.1-Hz breathing as intervention group or to HRV-Sham-BF as active control group. HRV-BF was performed for 4 weeks, whereas HRV was measured both during a short-term resting condition and during a paced breathing condition before and after intervention. Results: HRV-BF with 0.1-Hz breathing increased HRV and reduced panic symptoms in individuals with PD. HRV-BF with 0.1-Hz breathing demonstrated an increase in the time and frequency domain parameters of HRV during the short-term resting condition (ΔPost-Pre root mean square successive differences: 5.87 [14.03] milliseconds; ΔPost-Pre standard deviation of all NN intervals: 11.63 [17.06] milliseconds; ΔPost-Pre total power: 464.88 [1825.47] milliseconds²; ΔPost-Pre power in low-frequency range 0.04–0.15 Hz: 312.73 [592.71] milliseconds²), a decrease in the heart rate during the paced breathing condition (ΔPost-Pre: −5.87 [9.14] beats/min), and a decrease in the Panic and Agoraphobia Scale (ΔPost-Pre: −3.64 [6.30]). There was no intervention effect in the HRV-Sham-BF group. Conclusions: HRV-BF as a noninvasive and nonpharmacological treatment seems to be an important intervention option to improve reduced HRV and decrease panic symptoms in individuals with PD. Future studies are needed to establish whether these effects translate to reductions in the risk of cardiovascular disease in PD.