Sleep dysregulation in binge eating disorder and "food addiction": the orexin (hypocretin) system as a potential neurobiological link

Abstract

It has been proposed that binge eating reflects a pathological compulsion driven by the "addictive" properties of foods. Proponents of this argument highlight the large degree of phenomenological and diagnostic overlap between binge eating disorder (BED) and substance use disorders (SUDs), including loss of control over how much is consumed and repeated unsuccessful attempts to abstain from consumption, as well as commonalities in brain structures involved in food and drug craving. To date, very little attention has been given to an additional behavioral symptom that BED shares with SUDs-sleep dysregulation-and the extent to which this may contribute to the pathophysiology of BED. Here, we review studies examining sleep outcomes in patients with BED, which collectively point to a heightened incidence of sleep abnormalities in BED. We identify the orexin (hypocretin) system as a potential neurobiological link between compulsive eating and sleep dysregulation in BED, and provide a comprehensive update on the evidence linking this system to these processes. Finally, drawing on evidence from the SUD literature indicating that the orexin system exhibits significant plasticity in response to drugs of abuse, we hypothesize that chronic palatable food consumption likewise increases orexin system activity, resulting in dysregulated sleep/wake patterns. Poor sleep, in turn, is predicted to exacerbate binge eating, contributing to a cycle of uncontrolled food consumption. By extension, we suggest that pharmacotherapies normalizing orexin signaling, which are currently being trialed for the treatment of SUDs, might also have utility in the clinical management of BED.

Fig. 1. Binge-induced plasticity of orexin neurons contributes to the pathophysiology of BED.

We propose that binge eating results in orexin system plasticity similar to that induced by drugs of abuse, including increased hypothalamic orexin cell numbers, greater orexin input to reward and arousal centers, and greater reactivity to food-related stimuli. This general enhancement of orexin function is associated with the development of a hypermotivated state for food, which in turn increases proclivity to binge eat. Additionally, inappropriately high orexin system function results in hyperarousal and sleep dysregulation, which in turn promotes an increased risk of binge eating due to weakened inhibitory control, as a strategy to combat drowsiness during the daytime, and/or behavioral entrainment. Combined, this creates a self-promoting loop that serves to exacerbate the pathophysiology of BED. Thus, strategies that dampen orexin system signaling, such as orexin receptor antagonists, might be effective at breaking this loop and treating both dysregulated eating and sleep in BED.