Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body

Overview

Journal J Clin Endocrinol Metab

Publisher Oxford University Press

Specialty Endocrinology

Date 2015 Apr 17

PMID 25879513

Citations 39

Authors

Matthew S Tryon

Kimber L Stanhope

Elissa S Epel

Ashley E Mason

Rashida Brown

Valentina Medici

Peter J Havel

Kevin D Laugero

Affiliations

Soon will be listed here.

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.

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