Physiological responses to acute stress and the drive to eat: The impact of perceived life stress

Abstract

The stress-eating relationship is mediated by the release of cortisol from the hypothalamic pituitary adrenal (HPA) axis. Variability in stress-induced eating, and consequently, obesity, may be explained in part by individual differences in chronic stress, which disrupts the regulatory effects of the HPA axis on stress-induced eating. A greater understanding of the physiological mechanisms by which chronic stress affects acute stress-induced eating is critical in order to inform efforts to prevent and treat obesity. The current study examined the relationship between physiological responses to acute stress (cortisol and cardiovascular factors) and the drive to eat (ratings of hunger and desire to eat) in female undergraduates with high and low perceived life stress. Participants (n\u202f=\u202f64) rated their perceived life stress in an online screening and, on a separate visit, rated their drive to eat before and after a mental stress task. The present report focused on only participants in the lowest (n\u202f=\u202f16) and highest (n\u202f=\u202f14) quartiles of perceived life stress. Women with high perceived life stress showed greater stress-induced cortisol responses, but no significant changes in blood pressure or heart rate. The heightened cortisol responses were not associated with hunger and desire to eat, but the cardiovascular responses were positively associated with the drive to eat. Women with low perceived life stress showed no relationships between physiological stress markers and the drive to eat. These results suggest that the cortisol stress response is dissociated from the drive to eat in chronically stressed women, although due to the small sample size the data should be regarded as preliminary. Further studies are needed to explore how cortisol and cardiovascular reactivity affect stress-induced eating.