Abstract
The compulsive nature of weight loss behaviors central to anorexia nervosa (AN), such as relentless self-starvation and over-exercise, has led to the suggestion of parallels between AN and other compulsive disorders such as obsessive–compulsive disorder (OCD) and addictions. There is a huge unmet need for effective treatments in AN, which has high rates of morbidity and the highest mortality rate of any psychiatric disorder, yet a grave paucity of effective treatments. Viewing compulsivity as a transdiagnostic concept, seen in various manifestations across disorders, may help delineate the mechanisms responsible for the persistence of AN, and aid treatment development. We explore models of compulsivity that suggest dysfunction in cortico-striatal circuitry underpins compulsive behavior, and consider evidence of aberrancies in this circuitry across disorders. Excessive habit formation is considered as a mechanism by which initially rewarding weight loss behavior in AN may become compulsive over time, and the complex balance between positive and negative reinforcement in this process is considered. The physiological effects of starvation in promoting compulsivity, positive reinforcement, and habit formation are also discussed. Further research in AN may benefit from a focus on processes potentially underlying the development of compulsivity, such as aberrant reward processing and habit formation. We discuss the implications of a transdiagnostic perspective on compulsivity, and how it may contribute to the development of novel treatments for AN.
Highlights
Ventrolateral PFC in humans (Hampshire and Owen, 2006) impair performance on set-shifting tasks
WHAT IS THE NEURAL BASIS OF COMPULSIVITY? Models of the neurocircuitry involved in compulsive behavior suggest the involvement of a cortico-striatal circuit, consisting of a striatal and prefrontal component (Robbins, 2007; Brewer and Potenza, 2008; Fineberg et al, 2010)
This is distinct but related to an “impulsive” cortico-striatal circuit, involving the ventral striatum (VS)/nucleus accumbens (NAc), and the anterior cingulate cortex (ACC)/ventromedial prefrontal cortex. These compulsive and impulsive circuits are suggested to be intercommunicating, with the possibility that abnormalities in one circuit lead to abnormalities in the other (Fineberg et al, 2010). This is relevant for theories of dependence in which it is suggested that what may begin as impulsive behavior may eventually become compulsive with repetition of behavior, with a corresponding shift in control from impulsive to compulsive neural circuitry (Everitt and Robbins, 2005)
Summary
(43%; Dalle Grave et al, 2008). The presence of compulsive exercise in AN is extremely challenging to manage and can contribute to medically dangerous degrees of weight loss. Studies looking at decision making processes in AN, OCD, and substance dependence suggest in all three disorders a tendency to make disadvantageous decisions when choosing between immediate or long terms gains (Lawrence et al, 2006; Tchanturia et al, 2007b; Verdejo-Garcia et al, 2007) This impairment in decision making is suggested to be linked to the compulsive and self-destructive behavior seen across these disorders (Tchanturia et al, 2007b). Compulsive weight loss behavior, such as persistent food restriction and over-exercise, is a prominent feature of AN, and is parallel to the compulsive behaviors characteristic of OCD and substance dependence; with inevitable comorbidities If such parallels reflect similarities in the underlying mechanisms that drive this behavior, there should be some agreement about the neurobiological correlates of aberrant behavior across these disorders. Individuals with AN are often described as having low cognitive flexibility (Tchanturia et al, 2004), and consistently show www.frontiersin.org
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