I feel like Sisyphus — condemned to an eternity of rolling a boulder up a hill only to watch it roll down again each time I get it to the topA person describing what it’s like to have binge eating disorder.
Binge Eating Disorder (BED) affects 6.5 million Americans– more than anorexia nervosa and bulimia nervosa combined (Hudson, Hiripi, Pope, & Kessler, 2007). However, BED has historically received less attention from researchers and clinicians alike, with the disorder only officially recognized with the release of the DSM-5. Although many clients with BED receive treatment for other emotional problems, less than half have ever received treatment for binge eating (Hudson et al., 2007). It is essential that clinicians have the knowledge and tools to identify and intervene with this problem when it presents in clinical practice.
BED is characterized by recurrent periods in which an individual eats an amount of food that is significantly larger than would be eaten by others in similar circumstances and perceives a loss
of control over eating. These binge eating episodes must be associated with at least three additional criteria, including eating more quickly than normal, eating to the point of physical discomfort, eating large amounts of food when not hungry, eating alone due to embarrassment, and feeling remorse, disgust, or depression following the binge episode. In order to meet criteria for the DSM-5 diagnosis, these episodes must occur at least once a week for three months and cause distress, and cannot be accompanied by the compensatory behaviors seen in bulimia nervosa (American Psychiatric Association, 2013). Unlike other eating disorders, the overvaluation of weight and shape is not a diagnostic criterion for BED, but is associated with a greater severity of eating pathology and worse treatment prognosis (Grilo, 2013).
The identification of binge eating among clients may be impeded by several factors. First, the demographics of patients with BED differ substantially from other eating disorders. The gender difference is attenuated in comparison to other eating disorders, with 2.0% of men and 3.5% of women meeting criteria (Hudson et al., 2007). The mean age of onset is also later than other eating disorders, typically the mid-to-late twenties (Hudson et al., 2007), although later onsets are also observed. Observations of weight are also not a good indication of who is in need of treatment. BED is strongly associated with obesity, but is also diagnosed in individuals with a wide range of weights, shapes and sizes (Kessler, et al., 2013). Finally, a fear of stigma and shame, in part fueled by body image difficulties, negative social comparison and self-criticism (Duarte et al, 2016), may prevent individuals with BED from bringing these concerns forward to medical and psychological treatment providers (Hepworth & Paxton, 2007).
Etiology & Models
Understanding the etiology of BED may help both clients and clinicians overcome stigma associated with the disorder. It is likely that genetic vulnerability plays an important role, with heritability estimates ranging from 40% to 57% (Kessler, Hutson, Herman & Potenza, 2016). Multiple brain systems have been implicated, including both the opioid and dopamanergic systems (Kessler et al., 2016). There is some overlap between the neurobiological processes observed in BED and those observed in substance use disorders, leading some researchers to posit that BED may be an addiction to foods high in fat and sugar (Gearhardt, Davis, Kuschner, & Brownell, 2011). Despite similarities in some aspects of neurobiology and behavioral presentation, there are also important differences between these conditions. The impact of food on the brain is not as strong as it is for other misused substances, the neurological mechanisms regulating food intake are distributed more widely, and, perhaps most importantly for treatment, there are contraindications to utilizing an abstinence model in the treatment of BED (Schulte, Grilo & Gearhardt, 2016).
The most widely adopted models of BED suggest a central role for cognitive, behavioral, and interpersonal factors. The Transdiagnostic Model (Fairburn, Cooper & Shafran, 2003) posits that overvaluation of weight, shape, or control over eating contribute to dietary restraint that leads to binge eating. Perfectionism, low self-esteem, mood intolerance, and interpersonal difficulties are are believed to compound these difficulties among a subset of patients. A related model, known
as the Dual Pathway Model (Stice, 1994; Mason & Lewis, 2015), also suggests a key role for dietary restraint, but underscores the role of body shame and dissatisfaction in perpetuating dieting and highlights the role of negative affect and negative cognitions about food as a central triggers for binge eating episodes. Other models highlight the role of negative affect regulation in binge eating, positing that the intense focus during binge episodes temporarily blocks negative affect (Heatherton & Baumeister, 1991) or that the guilt following binge eating may be less aversive than the original source of negative mood (Kenardy, Arnow, & Agras, 1996).
The good news for providers is that there are effective, long lasting treatments for BED. Sharing this accurate narrative with clients, families, friends, doctors and dieticians will support more timely treatment. Psychotherapy in particular appears to lead to greater reductions in BE symptoms than either pharmacotherapy (Vocks et al., 2010) or behavioral weight loss programs (Wilson et al., 2010). A recent meta-analysis of binge eating treatments found medium to large effect sizes for psychotherapy and structured self-help (Vocks et al., 2010). Targeted adaptations of individual and group cognitive behavioral therapy, interpersonal therapy, and dialectical behavior therapy, as well as CBT in a guided self-help format, have all been demonstrated to lead to significant, stable improvements in binge eating (Hilbert et al., 2015; Telch, Agras, & Linehan, 2001), though treatment outcomes and dropout rates for individuals from minority racial/ethnic groups and for individuals from lower levels of education require further study (Thompson-Brenner et al, 2014).
With proper identification and the use of empirically-supported interventions, there is reason to be optimistic about recovery from BED. As clinicians, we can deliver this message and hold the hope for clients until they gain enough momentum in the recovery process to hold on to hope themselves.
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