The effect of weight suppression on attentional vigilance-avoidance for high-calorie food cues

2016 ◽  
Vol 108 ◽  
pp. 145
Author(s):  
Mooah Lee ◽  
Ji-Won Hur ◽  
Hyung-Jin Choi ◽  
Jang-Han Lee
2020 ◽  
Author(s):  
Yang Hu ◽  
Gang Ji ◽  
Guanya Li ◽  
Peter Manza ◽  
Wenchao Zhang ◽  
...  

Abstract The biological mediators that support cognitive-control and long-term weight-loss after laparoscopic sleeve gastrectomy (LSG) remain unclear. We measured peripheral appetitive hormones and brain functional-connectivity (FC) using magnetic-resonance-imaging with food cue-reactivity task in 25 obese participants at pre, 1 month, and 6 month after LSG, and compared with 30 normal weight controls. We also used diffusion-tensor-imaging to explore whether LSG increases brain structural-connectivity (SC) of regions involved in food cue-reactivity. LSG significantly decreased BMI, craving for high-calorie food cues, ghrelin, insulin, and leptin levels, and increased self-reported cognitive-control of eating behavior. LSG increased FC between the right dorsolateral prefrontal cortex (DLPFC) and the pregenual anterior cingulate cortex (pgACC) and increased SC between DLPFC and ACC at 1 month and 6 month after LSG. Reduction in BMI correlated negatively with increased FC of right DLPFC-pgACC at 1 month and with increased SC of DLPFC-ACC at 1 month and 6 month after LSG. Reduction in craving for high-calorie food cues correlated negatively with increased FC of DLPFC-pgACC at 6 month after LSG. Additionally, SC of DLPFC-ACC mediated the relationship between lower ghrelin levels and greater cognitive control. These findings provide evidence that LSG improved functional and structural connectivity in prefrontal regions, which contribute to enhanced cognitive-control and sustained weight-loss following surgery.


Appetite ◽  
2017 ◽  
Vol 116 ◽  
pp. 306-314 ◽  
Author(s):  
Selin Neseliler ◽  
Beth Tannenbaum ◽  
Maria Zacchia ◽  
Kevin Larcher ◽  
Kirsty Coulter ◽  
...  

2013 ◽  
Vol 120 ◽  
pp. 233-242 ◽  
Author(s):  
Matthew S. Tryon ◽  
Cameron S. Carter ◽  
Rashel DeCant ◽  
Kevin D. Laugero

Obesity ◽  
2013 ◽  
Vol 21 (10) ◽  
pp. 2029-2036 ◽  
Author(s):  
Shan Luo ◽  
Ana Romero ◽  
Tanja C. Adam ◽  
Houchun H. Hu ◽  
John Monterosso ◽  
...  

2018 ◽  
Vol 115 (48) ◽  
pp. E11238-E11247 ◽  
Author(s):  
Rebecca G. Boswell ◽  
Wendy Sun ◽  
Shosuke Suzuki ◽  
Hedy Kober

Obesity rates continue to rise alarmingly, with dire health implications. One contributing factor is that individuals frequently forgo healthy foods in favor of inexpensive, high-calorie, unhealthy foods. One important mechanism underlying these choices is food craving: Craving increases with exposure to unhealthy foods (and food cues, such as advertisements) and prospectively predicts eating and weight. Prior work has shown that cognitive regulation strategies that emphasize the negative consequences of unhealthy foods reduce craving. In Studies 1 and 2, we show that cognitive strategies also increase craving for healthy foods by emphasizing their positive benefits, and change food valuation (willingness to pay) for both healthy and unhealthy foods. In Studies 3 and 4, we demonstrate that brief training in cognitive strategies (“Regulation of Craving Training”; ROC-T) increases subsequent healthy (vs. unhealthy) food choices. This was striking because this change in food choices generalized to nontrained items. Importantly, in Study 5, we show that brief training in cognitive strategies also reduces food consumption by 93–121 calories. Consumed calories correlated with changes in food choice. Finally, in Study 6, we show that the training component of ROC-T is necessary, above and beyond any effect of framing. Across all studies (NTOTAL = 1,528), we find that cognitive strategies substantially change craving and food valuation, and that training in cognitive strategies improves food choices by 5.4–11.2% and reduces unhealthy eating, including in obese individuals. Thus, these findings have important theoretical, public health, and clinical implications for obesity prevention and treatment.


2021 ◽  
Vol 12 ◽  
Author(s):  
Sabrina Jones ◽  
Shan Luo ◽  
Hilary M. Dorton ◽  
Alexandra G. Yunker ◽  
Brendan Angelo ◽  
...  

It has been hypothesized that the incretin hormone, glucagon-like peptide-1 (GLP-1), decreases overeating by influencing mesolimbic brain regions that process food-cues, including the dorsal striatum. We previously showed that habitual added sugar intake was associated with lower glucose-induced circulating GLP-1 and a greater striatal response to high calorie food cues in lean individuals. Less is known about how dietary added sugar and obesity may interact to affect postprandial GLP-1 and its relationship to striatal responses to food cues and feeding behavior. The current study aimed to expand upon previous research by assessing how circulating GLP-1 and striatal food cue reactivity are affected by acute glucose consumption in participants with varied BMIs and amounts of habitual consumption of added sugar. This analysis included 72 participants from the Brain Response to Sugar Study who completed two study visits where they consumed either plain water or 75g glucose dissolved in water (order randomized; both drinks were flavored with non-caloric cherry flavoring) and underwent repeated blood sampling, a functional magnetic resonance imaging (fMRI) based food-cue task, and an ad-libitum buffet meal. Correlations between circulating GLP-1 levels, striatal food-cue reactivity, and food intake were assessed, and interactions between obesity and added sugar on GLP-1 and striatal responses were examined. An interaction between BMI and dietary added sugar was associated with reduced post-glucose GLP-1 secretion. Participants who were obese and consumed high levels of added sugar had the smallest increase in plasma GLP-1 levels. Glucose-induced GLP-1 secretion was correlated with lower dorsal striatal reactivity to high-calorie versus low-calorie food-cues, driven by an increase in reactivity to low calorie food-cues. The increase in dorsal striatal reactivity to low calorie food-cues was negatively correlated with sugar consumed at the buffet. These findings suggest that an interaction between obesity and dietary added sugar intake is associated with additive reductions in postprandial GLP-1 secretion. Additionally, the results suggest that changes to dorsal striatal food cue reactivity through a combination of dietary added sugar and obesity may affect food consumption.


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