Rose Seoyoung Chang1, Hilâl Cerit2, Taryn Hye1, E Leighton Durham1, Harlyn Aizley3, Sarah Boukezzi2, Florina Haimovici4, Jill M Goldstein5, Daniel G Dillon6, Diego A Pizzagalli7, Laura M Holsen8. 1. Division of Women's Health, Department of Medicine; 75 Francis St., Boston, MA, 02115, USA. 2. Division of Women's Health, Department of Medicine; 75 Francis St., Boston, MA, 02115, USA; Harvard Medical School, 25 Shattuck St., Boston, MA, 02115, USA. 3. Department of Psychiatry; 55 Fruit St., Boston, MA, 02114, USA. 4. Department of Psychiatry; Brigham and Women's Hospital, 75 Francis St., Boston, MA, 02115, USA; Harvard Medical School, 25 Shattuck St., Boston, MA, 02115, USA. 5. Division of Women's Health, Department of Medicine; 75 Francis St., Boston, MA, 02115, USA; Harvard Medical School, 25 Shattuck St., Boston, MA, 02115, USA; Department of Psychiatry; 55 Fruit St., Boston, MA, 02114, USA; Department of Obstetrics and Gynecology; 55 Fruit St., Boston, MA, 02114, USA; Innovation Center on Sex Differences in Medicine; Massachusetts General Hospital, 55 Fruit St., Boston, MA, 02114, USA. 6. Harvard Medical School, 25 Shattuck St., Boston, MA, 02115, USA; Center for Depression, Anxiety and Stress Research; 115 Mill St., Belmont, MA, 02478, USA. 7. Harvard Medical School, 25 Shattuck St., Boston, MA, 02115, USA; Center for Depression, Anxiety and Stress Research; 115 Mill St., Belmont, MA, 02478, USA; McLean Imaging Center; McLean Hospital, 115 Mill St., Belmont, MA, 02478, USA. 8. Division of Women's Health, Department of Medicine; 75 Francis St., Boston, MA, 02115, USA; Department of Psychiatry; Brigham and Women's Hospital, 75 Francis St., Boston, MA, 02115, USA; Harvard Medical School, 25 Shattuck St., Boston, MA, 02115, USA; Innovation Center on Sex Differences in Medicine; Massachusetts General Hospital, 55 Fruit St., Boston, MA, 02114, USA. Electronic address: lholsen@bwh.harvard.edu.
Abstract
BACKGROUND: Emotional eating has emerged as a contributing factor to overeating, potentially leading to obesity or disordered eating behaviors. However, the underlying biological mechanisms related to emotional eating remain unclear. The present study examined emotional, hormonal, and neural alterations elicited by an acute laboratory stressor in individuals with and without emotional eating. METHODS: Emotional (n = 13) and non-emotional eaters (n = 15) completed two main study visits, one week apart: one visit included a Stress version and the other a No-stress version of the Maastricht Acute Stress Task (MAST). Immediately pre- and post-MAST, blood was drawn for serum cortisol and participants rated their anxiety level. After the MAST, participants completed a Food Incentive Delay (FID) task during functional magnetic resonance imaging (fMRI), followed by an ad libitum snack period. RESULTS: Emotional eaters exhibited elevated anxiety (p = 0.037) and cortisol (p = 0.001) in response to the Stress MAST. There were no changes in anxiety or cortisol among non-emotional eaters in response to the Stress MAST or in either group in response to the No-stress MAST. In response to the Stress MAST, emotional eaters exhibited reduced activation during anticipation of food reward in mesolimbic reward regions (caudate: p = 0.014, nucleus accumbens: p = 0.022, putamen: p = 0.013), compared to non-emotional eaters. Groups did not differ in snack consumption. CONCLUSIONS: These data indicate disrupted neuroendocrine and neural responsivity to psychosocial stress amongst otherwise-healthy emotional eaters, who demonstrated hyperactive HPA-axis response coupled with hypoactivation in reward circuitry. Differential responsivity to stress may represent a risk factor in the development of maladaptive eating behaviors.
BACKGROUND: Emotional eating has emerged as a contributing factor to overeating, potentially leading to obesity or disordered eating behaviors. However, the underlying biological mechanisms related to emotional eating remain unclear. The present study examined emotional, hormonal, and neural alterations elicited by an acute laboratory stressor in individuals with and without emotional eating. METHODS: Emotional (n = 13) and non-emotional eaters (n = 15) completed two main study visits, one week apart: one visit included a Stress version and the other a No-stress version of the Maastricht Acute Stress Task (MAST). Immediately pre- and post-MAST, blood was drawn for serum cortisol and participants rated their anxiety level. After the MAST, participants completed a Food Incentive Delay (FID) task during functional magnetic resonance imaging (fMRI), followed by an ad libitum snack period. RESULTS: Emotional eaters exhibited elevated anxiety (p = 0.037) and cortisol (p = 0.001) in response to the Stress MAST. There were no changes in anxiety or cortisol among non-emotional eaters in response to the Stress MAST or in either group in response to the No-stress MAST. In response to the Stress MAST, emotional eaters exhibited reduced activation during anticipation of food reward in mesolimbic reward regions (caudate: p = 0.014, nucleus accumbens: p = 0.022, putamen: p = 0.013), compared to non-emotional eaters. Groups did not differ in snack consumption. CONCLUSIONS: These data indicate disrupted neuroendocrine and neural responsivity to psychosocial stress amongst otherwise-healthy emotional eaters, who demonstrated hyperactive HPA-axis response coupled with hypoactivation in reward circuitry. Differential responsivity to stress may represent a risk factor in the development of maladaptive eating behaviors.
Authors: Elissa Epel; Sherlyn Jimenez; Kelly Brownell; Laura Stroud; Catherine Stoney; Ray Niaura Journal: Ann N Y Acad Sci Date: 2004-12 Impact factor: 5.691
Authors: Valdo Ricca; Giovanni Castellini; Giulia Fioravanti; Carolina Lo Sauro; Francesco Rotella; Claudia Ravaldi; Lisa Lazzeretti; Carlo Faravelli Journal: Compr Psychiatry Date: 2011-05-26 Impact factor: 3.735
Authors: M F Dallman; S F Akana; A M Strack; K S Scribner; N Pecoraro; S E La Fleur; H Houshyar; F Gomez Journal: Ann N Y Acad Sci Date: 2004-06 Impact factor: 5.691