Effect of BMI and Binge Eating on Food Reward and Energy Intake: Further Evidence for a Binge Eating Subtype of Obesity

Background: Eating in the absence of hunger (EAH) measures intake of highly palatable, highly processed foods when sated, and may reflect food reward sensitivity. However, it is unknown whether EAH occurs in the presence of low-processed, nutrient-dense foods, and the relationship of self-reported food reward sensitivity with EAH during pregnancy has not been examined.Objective: This study tested whether EAH differs for highly-processed (HP) versus low-processed (LP) foods in pregnant women and examined relationships of EAH with self-reported food reward sensitivity and impulsivity.Design: Women in their 2nd trimester (n=46) enrolled in a counterbalanced crossover study in which they completed two EAH conditions following a standardized meal. Participants completed the Power of Food Scale (PFS), the modified Yale Food Addiction Scale (m-YFAS), and the Barratt Impulsiveness Scale (BIS). EAH energy intake (EAH-kcal) and proportion consumed (EAH-%) was measured overall and separately for sweet and savory test foods. Results: EAH-% was similar across conditions (16.3% ± 1.1% HP versus 17.9% ± 1.2% LP, P = 0.74), resulting in 347.7 ± 49.0 kcal greater energy intake in the HP versus LP condition (P < 0.001). PFS was not significantly associated with EAH; m-YFAS was positively associated with EAH-kcal and EAH-% of savory foods, and BIS was positively associated with EAH-kcal and EAH-% overall, and with EAH-% of sweet foods (p < 0.05). There was little evidence of an interaction of BIS with PFS or m-YFAS.Conclusions: Findings demonstrate that EAH in pregnant women correlates with self-reported food reward sensitivity and occurs for both highly processed and low-processed foods. Self-control did not modify the positive association of food reward sensitivity with eating beyond satiation in this sample.

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The Melanocortin System behind the Dysfunctional Eating Behaviors

Nutrients ◽

10.3390/nu12113502 ◽

2020 ◽

Vol 12 (11) ◽

pp. 3502

Author(s):

Emanuela Micioni Di Bonaventura ◽

Luca Botticelli ◽

Daniele Tomassoni ◽

Seyed Khosrow Tayebati ◽

Maria Vittoria Micioni Di Bonaventura ◽

...

Keyword(s):

Binge Eating ◽

Eating Behavior ◽

Energy Homeostasis ◽

Food Reward ◽

Eating Behaviors ◽

Clear Understanding ◽

Loss Of Function ◽

Melanocortin System ◽

Melanocortin 4 Receptor ◽

Underlying Mechanisms

The dysfunction of melanocortin signaling has been associated with obesity, given the important role in the regulation of energy homeostasis, food intake, satiety and body weight. In the hypothalamus, the melanocortin-3 receptor (MC3R) and melanocortin-4 receptor (MC4R) contribute to the stability of these processes, but MC3R and MC4R are also localized in the mesolimbic dopamine system, the region that responds to the reinforcing properties of highly palatable food (HPF) and where these two receptors seem to affect food reward and motivation. Loss of function of the MC4R, resulting from genetic mutations, leads to overeating in humans, but to date, a clear understanding of the underlying mechanisms and behaviors that promote overconsumption of caloric foods remains unknown. Moreover, the MC4R demonstrated to be a crucial modulator of the stress response, factor that is known to be strictly related to binge eating behavior. In this review, we will explore the preclinical and clinical studies, and the controversies regarding the involvement of melanocortin system in altered eating patterns, especially binge eating behavior, food reward and motivation.

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Genetic differences in the behavioral organization of binge eating, conditioned food reward, and compulsive-like eating in C57BL/6J and DBA/2J strains

10.1101/190827 ◽

2017 ◽

Cited By ~ 1

Author(s):

Richard K. Babbs ◽

Julia C. Kelliher ◽

Julia L. Scotellaro ◽

Kimberly P. Luttik ◽

Megan K. Mulligan ◽

...

Keyword(s):

Binge Eating ◽

Food Reward ◽

Drugs Of Abuse ◽

Bitter Taste ◽

Inbred Mouse ◽

Genetic Differences ◽

Mouse Strains ◽

Chromosome 6 ◽

Chromosome 11 ◽

Narrow Sense Heritability

ABSTRACTBinge eating (BE) is a heritable symptom of eating disorders associated with anxiety, depression, malnutrition, and obesity. Genetic analysis of BE could facilitate therapeutic discovery. We used an intermittent, limited access BE paradigm involving sweetened palatable food (PF) to examine genetic differences in BE, conditioned food reward, and compulsive-like eating between C57BL/6J (B6J) and DBA/2J (D2J) inbred mouse strains. D2J mice showed a robust escalation in intake and conditioned place preference for the PF-paired side. D2J mice also showed a unique style of compulsive-like eating in the light/dark conflict test where they rapidly hoarded and consumed PF in the preferred unlit environment. BE and compulsive-like eating exhibited narrow-sense heritability estimates between 56 and 73 percent. To gain insight into the genetic basis, we phenotyped and genotyped a small cohort of 133 B6J × D2J-F2 mice at the peak location of three quantitative trait loci (QTL) previously identified in F2 mice for sweet taste (chromosome 4: 156 Mb), bitter taste (chromosome 6: 133 Mb) and behavioral sensitivity to drugs of abuse (chromosome 11: 50 Mb). The D2J allele on chromosome 6 was associated with greater PF intake on training days and greater compulsive-like PF intake, but only in males, suggesting that decreased bitter taste may increase BE in males. The D2J allele on chromosome 11 was associated with an increase in final PF intake and slope of escalation across days. Future studies employing larger crosses and genetic reference panels comprising B6J and D2J alleles will identify causal genes and neurobiological mechanisms.

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