RESUMO
It is well known that stress elevates intake of total calories and shifts food preference toward unhealthy food choices. There is, however, little known on the physiological mechanisms that drive stress-induced hyperphagia. In order to better understand how to reduce stress eating, it is critical to identify mechanisms in humans that are points of convergence between stress and eating. The feeding-related hormones ghrelin, leptin, glucagon-like peptide-1 (GLP-1), and amylin are likely candidates. It was hypothesized that ghrelin, an orexigenic hormone, would increase in response to an acute laboratory stressor, but that leptin, GLP-1, and amylin (anorexigenic hormones) would decrease after stress. To this aim, participants (n = 47) came into the laboratory and had feeding-related hormones, salivary cortisol and α-amylase, and self-rated anxiety measured. Then they underwent either exposure to a stressor (n = 24), which reliably elevates measures of stress and energy intake, or a no-stress condition (n = 23). Feeding hormones, stress hormones, and self-rated anxiety were measured twice more after the stressor. Elevated self-rated anxiety and α-amylase confirmed the validity of the stressor. Furthermore, there was a time X condition interaction for both ghrelin and GLP-1. Ghrelin was significantly elevated after stress compared to baseline (p = .02) and there was a trend for GLP-1 to be higher in the stress condition over the no-stress condition immediately after the stressor (p = .07). Overall, ghrelin is the most likely candidate driving energy intake after stress in humans.
