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Randomized Controlled Trial
. 2015 Jun;100(6):2239-47.
doi: 10.1210/jc.2014-4353. Epub 2015 Apr 16.

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

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Free PMC article
Randomized Controlled Trial

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

Matthew S Tryon et al. J Clin Endocrinol Metab. .
Free PMC article

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.

Trial registration: ClinicalTrials.gov NCT01103921.

Figures

Figure 1.
Figure 1.
Metabolic-brain feedback model. Solid lines are stimulatory; dashed lines are inhibitory. During stress, the feed-forward actions of cortisol on brain stress pathways [eg, CRF, norepinephrine (NE)] promote palatable feeding, increase anxiety and fear, and stimulate activity in the sympathetic nervous system and HPA axis (6). Reduced feeding during stress decreases insulin, rendering cortisol, along with increased sympathetic nervous system outflow, catabolic in the periphery. Decreased energy storage disinhibits metabolic feedback and perpetuates the feed-forward actions of cortisol. However, with the ingestion of highly energetic comfort foods, increased cortisol stimulates insulin and energy storage, which feeds back to inhibit activity in the HPA axis and reduces cortisol output and its feed-forward effects, temporarily providing relief from stress. If the source of stress is not removed, continued self-medication in this fashion might lead to central obesity. Consistent with the concept that chronic stress increases allostatic load (23), the relative impact to brain stress pathways of the metabolic-feedback signal (ie, energy reserve or net anabolic activity) may decrease with chronic stress, thereby increasing the signal magnitude needed to impart its feedback effects; ie, tolerance might be developed. [Reproduced from M. Dallman et al: Chronic stress and obesity: a new view of “comfort food.” Proc Natl Acad Sci USA. 2003;100(20):11696–11701 (14), with permission. ©The Endocrine Society]
Figure 2.
Figure 2.
Montreal Imaging Stress Task experimental paradigm. The MIST paradigm was performed according to Pruessner et al (17) and consisted of a block design with two replicate runs. Each run lasted approximately 10 minutes and consisted of a rest, control, and experimental condition. Saliva samples for the examination of circulating free cortisol concentrations were taken upon arrival to the Imaging Research Center, 15 minutes later, immediately (time 0) prior to the first MIST run, and 15, 30, and 60 minutes (peak response) after the start of the first MIST run.
Figure 3.
Figure 3.
Effects of consuming sucrose and aspartame sweetened beverages on regional brain activity. A, Preintervention brain images showing effects of the stress task (MIST) at the preintervention visit, collapsed across all subjects from both intervention groups. The stress task led to significant (P < .01) unilateral (left panel) deactivation in the amygdala (−20, −4, −16), hippocampus (−22, −16, −22), and anterior cingulate cortex (BA10; −4, 52, 12). B, Repeated-measures ANCOVA showed a significant treatment group by visit interaction [F (1, 15) = 6.8, P = .020; effect size (η2p) = 0.15]. In contrast to the preintervention visit, significantly greater MIST-induced hippocampal activity was observed in the sucrose, but not aspartame, group at the postintervention visit. The brain image in panel C shows the net effect of sucrose consumption to increase above preintervention and the aspartame group hippocampal activity in response to the stress task (MIST). A higher number on the color scale indicates greater activity. *, P = .001 for statistical difference in hippocampal activity between sucrose and aspartame groups at the postintervention visit.
Figure 4.
Figure 4.
Effects of consuming sucrose- and aspartame-sweetened beverages on MIST-induced cortisol. A, The mean ± SE stress task (MIST) induced plasma cortisol concentration change before (preintervention) and 2 weeks after (postintervention) daily (three times per day) consumption of sucrose or aspartame-sweetened beverages. Δ-Cortisol was calculated as the difference between the cortisol values before (0 min) induction of the first MIST run and after the second MIST run was completed (60 min). We included the prestress cortisol concentration and prestress cortisol concentration × visit day terms in the repeated-measures statistical model. As supported by a significant treatment group × visit interaction [F (1, 15) = 4.7, P = .048; effect size (η2p) = 0.36], the cortisol response to the stress task (MIST) was diminished after 2 weeks of consuming sucrose but not aspartame. Log-transformed cortisol concentrations at each sample time are shown for the preintervention (B) and postintervention (C) visits. *, P = .024 for statistical difference in δ-cortisol between sucrose and aspartame groups at the postintervention visit.

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