scholarly journals Stress Responsiveness and Emotional Eating Depend on Youngsters’ Chronic Stress Level and Overweight

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3654
Author(s):  
Kathleen Wijnant ◽  
Joanna Klosowska ◽  
Caroline Braet ◽  
Sandra Verbeken ◽  
Stefaan De Henauw ◽  
...  

The persistent coexistence of stress and paediatric obesity involves interrelated psychophysiological mechanisms, which are believed to function as a vicious circle. Here, a key mechanistic role is assumed for stress responsiveness and eating behaviour. After a stress induction by the Trier Social Stress Test in youngsters (n = 137, 50.4% boys, 6–18 years), specifically those high in chronic stress level and overweight (partial η2 = 0.03–0.07) exhibited increased stress vulnerability (stronger relative salivary cortisol reactivity and weaker happiness recovery) and higher fat/sweet snack intake, compared to the normal-weight and low-stress reference group. Stress responsiveness seems to stimulate unhealthy and emotional eating, i.e., strong cortisol reactivity was linked to higher fat/sweet snack intake (β = 0.22) and weak autonomic system recovery was linked to high total and fat/sweet snack intake (β = 0.2–0.3). Additionally, stress responsiveness acted as a moderator. As a result, stress responsiveness and emotional eating might be targets to prevent stress-induced overweight.

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Christine Fahrngruber ◽  
Kalina Duszka ◽  
Jürgen König

AbstractChronic stress is associated with impacting eating behavior, namely food choice and energy intake, with a shift towards more palatable and energy dense foods. Additionally, eating behavior is influenced by other psychological factors like mood and emotions. The categorization of people into eating types such as restrained, emotional, and external eaters has gained attraction. Reported changes in eating behavior due to psychological stress are only occasionally accompanied by measures of physiological hunger through ghrelin. The primary objective of this study was to investigate how chronic stress and acute cortisol reactivity affect active ghrelin secretion and how these outcomes account for different eating types. 16 healthy, young males (age: 23 ± 3 years, BMI: 22.5 ± 1.3kg/m2) with low (n = 8) and average-to-high (n = 8) chronic stress level were subjected to the Trier Social Stress Test (TSST) and a control version on two separate days. Active ghrelin, cortisol, glucose, and heart rate were measured throughout the test. Subjects rated their hunger by means of visual analog scale and current mood was assessed with the Positive and Negative Affect Scale (PANAS). In addition, participants filled out the Dutch Eating Behavior Questionnaire (DEBQ) to account for their subjective eating behavior. Overall ghrelin values where higher on the test day compared to the control day. Ghrelin values were also higher during the time leading up to the stress or control test (TSST) than during the conclusion of said tests. On both days, mean values for active ghrelin where higher in individuals with low chronic stress exposure compare to those with average-to-high chronic stress exposure. While values from test to control day decreased for lower stressed participants, they slightly increased for higher stressed participants. Cortisol responders displayed higher ghrelin values on test day than cortisol non-responders, but this association inverted for the control day. Results indicate that chronic stress influences acute stress response and further alters active ghrelin production, which in turn can influence eating behavior. Replication in a greater group of participants of differing weight and sex could yield a greater understanding of stress induced eating. Factors such as relaxation techniques and coping mechanisms could further improve our knowledge and evaluate treatment possibilities.


2009 ◽  
Vol 21 (1) ◽  
pp. 69-85 ◽  
Author(s):  
Megan R. Gunnar ◽  
Sandi Wewerka ◽  
Kristin Frenn ◽  
Jeffrey D. Long ◽  
Christopher Griggs

AbstractHome baseline and laboratory stressor (Trier Social Stress Test for Children) measures of salivary cortisol were obtained from 82 participants (40 girls) aged 9, 11, 13, and 15 years. Measures of pubertal development, self-reported stress, parent reports of child depressive symptoms and fearful temperament, and cardiac measures of sympathetic and parasympathetic activity were also obtained. Significant increases in the home cortisol baselines were found with age and pubertal development. Cortisol stress reactivity differed by age group with 11-year-olds and 13-year-old boys showing blunted reactivity and 9-year-olds, 13-year-old girls, and 15-year-olds showing significant cortisol reactions. Cortisol reactivity correlated marginally with sexual maturation. Measures of sympathetic activity revealed increased sympathetic modulation with age. Higher sympathetic tone was associated with more fearful temperament, whereas greater cortisol reactivity was associated with more anxious and depressed symptoms for girls. The importance of these findings for the hypothesis that puberty-associated increases in hypothalamic–pituitary–adrenal axis activity heightens the risk of psychopathology is discussed.


2011 ◽  
Vol 36 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Ayala Fridman ◽  
Marinus H. van IJzendoorn ◽  
Abraham Sagi-Schwartz ◽  
Marian J. Bakermans-Kranenburg

In the current study we tested whether ADRA2B moderates stress regulation of Holocaust survivors as indexed by their diurnal cortisol secretion and cortisol reactivity to a stressor. Salivary cortisol levels of 54 female Holocaust survivors and participants in the comparison group were assessed during a routine day and in response to a stress-evoking procedure (an adapted version of the Trier Social Stress Test [TSST]). ADRA2B did not moderate differences between Holocaust survivors and participants in the comparison group in terms of cortisol reactivity to the TSST. Holocaust survivors with the wildtype ADRA2B, however, displayed higher diurnal cortisol levels than did participants in the comparison group with the same genotype, whereas no difference was found between these groups in carriers of the deletion variant, previously associated with more reexperiencing of traumatic events. Carriers of the deletion variant might have been driven in the long run to resolve their vividly remembered experiences, and therefore currently show less stress dysregulation as evident from their cortisol levels.


2017 ◽  
Vol 6 (3) ◽  
pp. 301-314 ◽  
Author(s):  
Raegan Mazurka ◽  
Katherine E. Wynne-Edwards ◽  
Kate L. Harkness

Two of the most robust findings in depression research are (a) that women are twice as likely to become depressed than men and (b) that stress is an important risk factor for depression. Although sex differences in stress reactivity may be an important determinant of differential risk for depression, few studies have examined sex differences in neurobiological reactivity to stress. The purpose of the current study was to assess sex differences in the HPA axis response to stress in depressed versus healthy controls by comparing the cortisol response to the Trier Social Stress Test in a community sample of adolescents (ages 12–18). Depressed boys showed significantly heightened cortisol reactivity compared with depressed girls, whose response was blunted compared with nondepressed girls. This diverging pattern of cortisol reactivity to stress among depressed girls and boys may help to explain the sex difference in depression prevalence that emerges during the adolescent period.


2010 ◽  
Vol 35 (9) ◽  
pp. 1397-1403 ◽  
Author(s):  
Peter Jönsson ◽  
Mattias Wallergård ◽  
Kai Österberg ◽  
Åse Marie Hansen ◽  
Gerd Johansson ◽  
...  

2020 ◽  
pp. 1-12 ◽  
Author(s):  
Ethan S. Young ◽  
Jenalee R. Doom ◽  
Allison K. Farrell ◽  
Elizabeth A. Carlson ◽  
Michelle M. Englund ◽  
...  

Abstract Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.


2020 ◽  
Vol 32 (5) ◽  
pp. 1854-1863
Author(s):  
Nicole B. Perry ◽  
Carrie E. DePasquale ◽  
Bonny Donzella ◽  
Megan R. Gunnar

AbstractMegan Gunnar's pubertal stress recalibration hypothesis was supported in a recent study of previously institutionalized (PI) youth such that increases in pubertal stage were associated with increases in cortisol stress reactivity. This work provides evidence that puberty may open up a window of recalibration for PI youth, resulting in a shift from a blunted to a more typical cortisol stress response. Using the same sample (N = 132), the current study aimed to elucidate whether increases in cortisol are associated with increases in adaptive functioning or whether they further underlie potential links to developmental psychopathology. Specifically, we examined the bidirectional associations between cortisol stress reactivity and both internalizing and externalizing symptoms across three timepoints during the pubertal period. Youth reported on their own internalizing symptoms and parents reported on youths’ externalizing symptoms. Cortisol reactivity was assessed during the Trier social stress test. Analyses revealed no associations between cortisol reactivity and externalizing symptoms across puberty for PI youth. However, longitudinal bidirectional associations did emerge for internalizing symptoms such that increases in cortisol reactivity predicted increases in internalizing symptoms and increases in internalizing symptoms predicted increases in cortisol reactivity. Findings suggest that recalibrating to more normative levels of cortisol reactivity may not always be associated with adaptive outcomes for PI youth.


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