Matthew S Tryon1, Kimber L Stanhope1, Elissa S Epel1, Ashley E Mason1, Rashida Brown1, Valentina Medici1, Peter J Havel1, Kevin D Laugero1. 1. Departments of Nutrition (M.S.T., K.L.S., K.D.L., P.J.H.) and Molecular Biosciences (P.J.H.), School of Veterinary Medicine, and Division of Gastroenterology and Hepatology (V.M.), School of Medicine, University of California, Davis, and Stress Biology and Nutrition Research Laboratory (K.D.L.), Obesity and Metabolism Research Unit, Western Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, Davis, California 95616; and Department of Psychiatry (E.S.E., A.E.M., R.B.), University of California, San Francisco, San Francisco, California 94143.
Abstract
CONTEXT: Sugar overconsumption and chronic stress are growing health concerns because they both may increase the risk for obesity and its related diseases. Rodent studies suggest that sugar consumption may activate a glucocorticoid-metabolic-brain-negative feedback pathway, which may turn off the stress response and thereby reinforce habitual sugar overconsumption. OBJECTIVE: The objective of the study was to test our hypothesized glucocorticoid-metabolic-brain model in women consuming beverages sweetened with either aspartame of sucrose. DESIGN: This was a parallel-arm, double-masked diet intervention study. SETTING: The study was conducted at the University of California, Davis, Clinical and Translational Science Center's Clinical Research Center and the University of California, Davis, Medical Center Imaging Research Center. PARTICIPANTS: Nineteen women (age range 18-40 y) with a body mass index (range 20-34 kg/m(2)) who were a subgroup from a National Institutes of Health-funded investigation of 188 participants assigned to eight experimental groups. INTERVENTION: The intervention consisted of sucrose- or aspartame-sweetened beverage consumption three times per day for 2 weeks. MAIN OUTCOME MEASURES: Salivary cortisol and regional brain responses to the Montreal Imaging Stress Task were measured. RESULTS: Compared with aspartame, sucrose consumption was associated with significantly higher activity in the left hippocampus (P = .001). Sucrose, but not aspartame, consumption associated with reduced (P = .024) stress-induced cortisol. The sucrose group also had a lower reactivity to naltrexone, significantly (P = .041) lower nausea, and a trend (P = .080) toward lower cortisol. CONCLUSION: These experimental findings support a metabolic-brain-negative feedback pathway that is affected by sugar and may make some people under stress more hooked on sugar and possibly more vulnerable to obesity and its related conditions.
RCT Entities:
CONTEXT: Sugar overconsumption and chronic stress are growing health concerns because they both may increase the risk for obesity and its related diseases. Rodent studies suggest that sugar consumption may activate a glucocorticoid-metabolic-brain-negative feedback pathway, which may turn off the stress response and thereby reinforce habitual sugar overconsumption. OBJECTIVE: The objective of the study was to test our hypothesized glucocorticoid-metabolic-brain model in women consuming beverages sweetened with either aspartame of sucrose. DESIGN: This was a parallel-arm, double-masked diet intervention study. SETTING: The study was conducted at the University of California, Davis, Clinical and Translational Science Center's Clinical Research Center and the University of California, Davis, Medical Center Imaging Research Center. PARTICIPANTS: Nineteen women (age range 18-40 y) with a body mass index (range 20-34 kg/m(2)) who were a subgroup from a National Institutes of Health-funded investigation of 188 participants assigned to eight experimental groups. INTERVENTION: The intervention consisted of sucrose- or aspartame-sweetened beverage consumption three times per day for 2 weeks. MAIN OUTCOME MEASURES: Salivary cortisol and regional brain responses to the Montreal Imaging Stress Task were measured. RESULTS: Compared with aspartame, sucrose consumption was associated with significantly higher activity in the left hippocampus (P = .001). Sucrose, but not aspartame, consumption associated with reduced (P = .024) stress-induced cortisol. The sucrose group also had a lower reactivity to naltrexone, significantly (P = .041) lower nausea, and a trend (P = .080) toward lower cortisol. CONCLUSION: These experimental findings support a metabolic-brain-negative feedback pathway that is affected by sugar and may make some people under stress more hooked on sugar and possibly more vulnerable to obesity and its related conditions.
Authors: Mary F Dallman; Norman C Pecoraro; Susanne E La Fleur; James P Warne; Abigail B Ginsberg; Susan F Akana; Kevin C Laugero; Hani Houshyar; Alison M Strack; Seema Bhatnagar; Mary E Bell Journal: Prog Brain Res Date: 2006 Impact factor: 2.453
Authors: Yvonne M Ulrich-Lai; Michelle M Ostrander; Ingrid M Thomas; Benjamin A Packard; Amy R Furay; C Mark Dolgas; Daniella C Van Hooren; Helmer F Figueiredo; Nancy K Mueller; Dennis C Choi; James P Herman Journal: Endocrinology Date: 2007-01-04 Impact factor: 4.736
Authors: Michelle T Foster; James P Warne; Abigail B Ginsberg; Hart F Horneman; Norman C Pecoraro; Susan F Akana; Mary F Dallman Journal: Endocrinology Date: 2008-12-23 Impact factor: 4.736
Authors: Elissa S Epel; Alexandra D Crosswell; Stefanie E Mayer; Aric A Prather; George M Slavich; Eli Puterman; Wendy Berry Mendes Journal: Front Neuroendocrinol Date: 2018-03-15 Impact factor: 8.606