Tryon MS, Stanhope KL, Epel ES, Mason AE, Brown R, Medici V, Havel PJ, Laugero KD. (2015) J Clin Endocrinol Metab. DOI: http://dx.doi.org/10.1210/jc.2014-4353
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.
The objective of the study was to test our hypothesized glucocorticoid-metabolic-brain model in women consuming beverages sweetened with either aspartame of sucrose.
This was a parallel-arm, double-masked diet intervention study.
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.
Nineteen women (age range 18-40 y) with a body mass index (range 20-34 kg/m2) who were a subgroup from a National Institutes of Health-funded investigation of 188 participants assigned to eight experimental groups.
The intervention consisted of sucrose- or aspartame-sweetened beverage consumption three times per day for 2 weeks.
Salivary cortisol and regional brain responses to the Montreal Imaging Stress Task were measured.
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.
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.