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Title:   Author  item
                                            TRYON, MATTHEW - University Of Californiaitem
                                            STANHOPE, KIMBER - University Of Californiaitem
                                            EPEL, ELISSA - University Of Californiaitem
                                            MASON, ASHLEY - University Of Californiaitem
                                            BROWN, RASHIDA - University Of Californiaitem
                                            MEDICI, VALENTINA - University Of Californiaitem
                                            HAVEL, PETER - University Of Californiaitem
                                            Laugero, Kevin
  Submitted to: Journal of Clinical Endocrinology and Metabolism
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 3/30/2015
                                    Publication  Date: 6/1/2015
                                    Citation: Tryon, M.S., Stanhope, K.L., Epel, E.S., Mason, A.E., Brown, R., Medici, V., Havel, P.J., Laugero, K.D. 2015. Excessive sugar consumption may be a difficult habit to break: a view from the brain and body. Journal of Clinical Endocrinology and Metabolism. 100(6):2239-2247. https://doi.org/10.1210/jc.2014-4353.DOI: https://doi.org/10.1210/jc.2014-4353                                                              
                                Interpretive Summary: Sugar overconsumption and chronic stress are growing health concerns because they both may increase risk for obesity and related diseases.  We previously hypothesized a metabolic-brain feedback pathway as a physiological basis for stress eating and link between stress, a habit of excessive sugar consumption, and risk for obesity and related diseases.  Here, we provide novel evidence supporting this model in humans.  We report results from a two week intervention comparing the neural (fMRI) and neuroendocrine effects of consuming sucrose and aspartame sweetened beverages.   Our results provide the first evidence from humans that high sugar, but not aspartame, consumption may provide relief from stress by suppressing neural and cortisol stress responses.  These experimental findings support a metabolic-brain negative feedback pathway that is affected by sugar and may make some people under stress more susceptible to a habit of sugar overconsumption and its negative effects on health.
                                Technical Abstract: Importance:  Sugar overconsumption and chronic stress are growing health concerns because they both may increase risk for obesity and related disease.  Psychological or emotional stress may trigger habitual overconsumption of sugar and amplify the detrimental health effects of sugar consumption. The physiological basis for stress-induced sugar consumption is unknown.  Studies in rodents suggest a metabolic negative feedback involving the brain and hypothalamic-pituitary-adrenal (HPA) axis whereby sugar consumption inhibits stress-induced neuroendocrine reactivity. Objective:  Compare the effects of daily sucrose or aspartame consumption on stress-induced neuronal (fMRI) and HPA (cortisol) responses in humans.  Design, Setting, and Participants:  Nineteen healthy adult women participated in a parallel-arm, double-blinded diet intervention.  Women consumed sucrose- or aspartame-sweetened beverages with each meal (3X/d) for 2 weeks.  Before and after the intervention, women underwent the Montreal Imaging Stress Task (MIST) at the UC Davis Imaging Research Center and a separate session of naltrexone-induced endogenous opioid blockade (at home). Saliva was collected for cortisol analysis during the MIST and naltrexone experiments.  Main Outcome Measures:  MIST-induced regional brain activation and MIST- and naltrexone-induced cortisol responses.  Results:  Comparing aspartame and sucrose groups, there were no differences in MIST patterns of brain activation between groups at pre-intervention but the sucrose group at post-intervention had significantly higher activity in the left hippocampus (P = 0.001).  No differences in stress-induced MIST cortisol were observed at pre-intervention but, as expected, stress-induced cortisol was lower (P = 0.024) in the sucrose group by 110% at post-intervention.  The sucrose group also had lower reactivity to naltrexone – a trend (P = 0.080) toward lower cortisol and significantly (P = 0.041) lower nausea.  Conclusion and Relevance:   Our findings provide the first evidence from humans that high sugar consumption may provide relief from stress by suppressing the neural and peripheral stress response. This in turn could reinforce the drive to consume sugar. While the hippocampus deactivation during stress typically permits high cortisol release, sugar dampens the stress response by activating the hippocampus during stress.  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.


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