Stress-induced eating may be a critical risk factor for the development of obesity in youth. Stress- related activation of the hypothalamic-pituitary-adrenal (HPA) axis and consequent elevations in cortisol play a central role in stress-induced eating. Adolescence is a key developmental period to examine the stress-eating association as it is marked by increased vulnerability to stress and high probability of sustained obesity into adulthood. Low-income adolescents are a particularly high-risk group in this regard and may be especially susceptible to stress-induced eating given the stressful environments in which they live (e.g., neighborhood violence) and vulnerability to eating-specific stressors (e.g., insufficiet food availability). However, the small body of available research on stress-induced eating in youth is limited by 1) failure to examine how cortisol response and patterns of emotional eating interact to impact dietary intake following stress in youth, 2) failure to experimentally manipulat the effects of exposure to a stressor on energy intake in lean versus obese adolescents, and 3) the focus on economically homogenous samples of middle-income families. The proposed study extends the understanding of biobehavioral processes underlying stress-induced eating in youth by concurrently examining associations between cortisol reactivity, emotional eating and objective energy intake in obese and lean low-income adolescents, using a validated experimental paradigm (Trier Social Stress Test for Children;TSST-C) known to produce elevations in cortisol in adolescents. Our preliminary data suggest that obese adolescents show greater cortisol reactivity to the TSST-C compared to lean adolescents. The proposed R03 will compare energy intake in obese (n = 40) and lean (n = 40) low- income adolescents (12-17 years) following stress induction versus a control day.
Specific Aims are to: (1) determine if low-income obese adolescents differ from low-income lean adolescents in cortisol reactivity to stress-induction, (2) determine if energy intake following stress is more strongly related to cortisol reactivity among low-income adolescents who score higher on emotional eating, and (3) explore whether cortisol stress reactivity or perceived stress is more predictive of energy intake in adolescents. Consistent with the mission of the NICHD Obesity Research Strategic Core, findings from this study will provide a strong foundation for a programmatic line of research designed to examine the role of cortisol reactivity and emotional eating in the development of obesity in low-income adolescents. The potential public health impact of this study is significant, given that findings will help to identify a subgroup of low-income adolescents at heightened risk for obesity. Perhaps equally important, these data will inform the development of new or augmented interventions tailored for low-income adolescents who are exposed to high-stress environments, by identifying specific physiologic pathways (HPA axis activation) and behavioral patterns (emotional eating) that put these youth at risk for obesity and can be targeted to enhance behavioral weight control intervention.
Stress-related activation of the hypothalamic-pituitary-adrenal (HPA) axis and resulting elevations in the stress hormone cortisol play a critical role in stress-induced eating, which may be a critical risk factor for the development of obesity and type 2 diabetes. The proposed study adopts a novel approach to understanding stress-induced eating in low-income adolescents who are at increased risk for obesity and face high-stress environments associated with poverty by examining how emotional eating interacts with cortisol stress reactivity to influence objective energy intake following stress in obese and lean low-income adolescents. Results from this study will be used to identify a sub-group of low-income adolescents who are at heightened risk for obesity and to inform the development of therapeutic interventions to decrease stress-induced eating as part of obesity prevention and intervention in low-income adolescents.
