Abstract
Reward mechanisms are likely implicated in the pathophysiology of binge-eating behaviour, which is a key symptom of binge-eating disorder (BED). Since endocannabinoids modulate food-related reward, we aimed to investigate the responses of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) to hedonic eating in patients with BED. Peripheral levels of AEA and 2-AG were measured in 7 obese BED patients before and after eating favorite (hedonic eating) and non-favorite (non-hedonic eating) foods. We found that plasma levels of AEA progressively decreased after eating the non-favorite food and significantly increased after eating the favorite food, whereas plasma levels of 2-AG did not differ significantly between the two test conditions, although they showed a trend toward significantly different time patterns. The changes in peripheral AEA levels were positively correlated to the subjects’ sensations of the urge to eat and the pleasantness while eating the presented food, while changes in peripheral 2-AG levels were positively correlated to the subjects’ sensation of the pleasantness while eating the presented food and to the amount of food they would eat. These results suggest the occurrence of distinctive responses of endocannabinoids to food-related reward in BED. The relevance of such findings to the pathophysiology of BED remains to be elucidated.
Highlights
In the last edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) [1]binge-eating disorder (BED) has been formally recognized as a distinctive eating disorder
In the former case, energy deprivation generates homeostatic hunger, which drives eating in order to remove energy deficit; in the latter case, especially when highly palatable foods are available in the environment, hedonic hunger may generate and drive the consumption of food exclusively to obtain reward from food in spite of no energy need [3]
Accumulating evidence suggests that food-related reward is exerted through brain motivation–reward pathways, and that most of the modulators of homeostatic eating participate in the control of the rewarding component of food intake [4]
Summary
Binge-eating disorder (BED) has been formally recognized as a distinctive eating disorder It is characterized by episodes of consuming an unusually large amount of food within a discrete period of time, accompanied by a sense of lack of control over eating, without the recurrent use of inappropriate compensatory behaviors as in bulimia nervosa. Accumulating evidence suggests that food-related reward is exerted through brain motivation–reward pathways, and that most of the modulators of homeostatic eating participate in the control of the rewarding component of food intake [4]. Among those endogenous biochemical mediators, endocannabinoids, i.e., arachidonoylethanolamide (anandamide, AEA) and 2-arachidonoylglycerol (2-AG), have been shown to modulate both homeostatic and rewarding aspects of food intake by stimulating brain cannabinoid CB1 receptors [5,6]
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