Psychosocial stress may lead to increased food consumption and overweight. In turn, obesity is related to reduced brain energy content. We hypothesized that psychosocial stress influencing food intake may alter the neuroenergetic status in the human brain. We tested 14 healthy normal weight men in a randomized crossover design. A modified version of the Trier Social Stress Test (TSST) was carried out to induce psychosocial stress vs. control in a neuroimaging setting. Cerebral energy content, i.e. high energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr), was measured by 31phosphorus magnetic resonance spectroscopy. Food intake was quantified by an ad libitum buffet test. Stress hormonal response and alterations in glucose metabolism were monitored by blood sampling. Before data collection, we mainly expected a stress-induced reduction in cerebral high energy phosphates, followed by higher food intake. Psychosocial stress increased serum cortisol concentrations (p = .003) and fat intake of all participants by 25% (p = .043), as well as food intake of "stress-eaters" by 41.1% (p = .003) compared with controls. Blood glucose and insulin concentrations were not affected (p > .174 for both). Cerebral ATP and PCr levels generally increased upon stress-induction (p > = .022 and p = .037, respectively). Our data confirm that psychosocial stress may enhance food intake. Contrary to our expectations, stress induces a distinct increase in the neuroenergetic status. This insight suggests that the underlying central nervous mechanisms of stress-induced overeating may involve the regulation of the brain energy homeostasis.
Keywords: Eating behavior; HPA-axis; Trier Social Stress Test (TSST); adenosine triphosphate (ATP); phosphocreatine (PCr).