What is Binge-Eating Disorder?
We’ve so far discussed anorexia nervosa and bulimia nervosa this week, as we honor National Eating Disorders Awareness Week with a review on a different eating disorder each day. Today’s comes a day late, so I will try and get the next one out and get us all caught up and on schedule. We’re discussing binge-eating disorder today, which will draw a lot from the last review, on bulimia, but has a lot of different insights you’ll be able to learn from. I hope you enjoy this one!
Definition and Diagnosis
Binge-eating disorder (BED) is a relatively new eating disorder, at least as far as the DSM is concerned. In the DSM-IV, BED was listed as an Eating Disorder Not Otherwise Specified (EDNOS; now called “Otherwise Specified Feeding or Eating Disorder,” or “OSFED”). It also had no severity ranking method. This is because, at the time, both the size and scope of the available literature, and the available research tools, were limited. In the DSM 5, the most current edition, BED is now listed as its own distinct ED, with its own severity ranking scale.
To be diagnosed with BED, the DSM requires 5 qualifications:
Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:
Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than most people would eat in a similar period of time under similar circumstances
The sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating)
Binge-eating episodes are associated with three (or more) of the following:
Eating much more rapidly than normal
Eating until feeling uncomfortably full
Eating large amounts of food when not feeling physically hungry
Eating alone because of being embarrassed by how much one is eating
Feeling disgusted with oneself, depressed, or very guilty after overeating
Marked distress regarding binge eating is present.
The binge eating occurs, on average, at least 1 day a week for 3 months.
The binge eating is not associated with the regular use of inappropriate compensatory behavior (e.g., purging, fasting, excessive exercise) and does not occur exclusively during the course of anorexia nervosa or bulimia nervosa.
Severity is ranked based on frequency of binge episodes:
Mild: Average of 1-3 binge episodes a week
Moderate: Average of 4-7 binge episodes a week
Severe: Average of 8-13 binge episodes a week
Extreme: Average of 14 or more binge episodes a week
Diagnosing BED presents some unique difficulties for both the medical provider and the patient, as distinguishing objective and subjective binge experiences can make a clear diagnosis tricky (Wolfe et al., 2009).
The history of binge eating behaviors is essentially the exact same as that of bulimic behaviors. The non-purging component of BED was actually a more novel concept than the original notion of binge-purge behaviors, which can be traced back to the 12th and 13th centuries, as a practice used by royalty and those in the highest classes.
It wasn’t until 1959 that binge-eating disorder was officially named. Dr. Albert Stunkard originally described it and, interestingly, linked it to night-eating syndrome (NES) symptoms. NES is now listed in the DSM 5 under OSFED, and it does not necessarily require a binge eating component for diagnosis.
Binge eating symptoms were first included in official medical diagnostic criteria in 1987 with the release of the DSM-III-R (the revised DSM-III), but they were listed as symptoms of BN, rather than their own eating disorder. As mentioned earlier, in the next edition of the DSM, BED was recognized as separate from BN but was only listed as an EDNOS. Finally, in our current edition, the DSM 5, BED has been officially listed as its own distinct disorder.
2.8% of the population has BED, rendering it the most common eating disorder among adults, but this is only based on DSM-IV diagnostic criteria, so it is likely higher when using DSM 5 criteria (Hudson et al., 2007). In the former DSM, binge eating had to occur twice a week for at least six months, but in the current edition, this was dropped down to once a week for at least three months. Not to mention, its listing as its own distinct eating disorder changes the mode of diagnosis for the millions who suffer from it.
While BED is most common in obese and overweight individuals, weight has nothing to do with the diagnosis and nonobese individuals are just as likely to suffer from this (Bruce & Wilfley, 1996). As well, not all obese individuals have binge eating behaviors, which is an important point to mention, as binge eating is a specific pathological behavior and not the simple act of overeating it is so frequently portrayed as.
Etiology and Pathophysiology
In looking deeper into the etiology of BED, it is most useful to look at the most common comorbidities. These would include clinical depression (Hudson et al., 2007), disproportionate internalization of weight bias (Pearl, White & Grilo, 2014), low self-esteem, poor body image (which does not need to exist in accordance with overweight or obesity), and loss-of-control (LOC) eating patterns.
The pathogenic model Fairburn outlined for BN has been translated into implications for BED. In the case of binge eating, this model posits that body image-related low self-esteem generates anxiety and negative affect that results in excessive dieting and restrictive behaviors, which ultimately trigger binge eating (Fairburn, Cooper & Shafran, 2003; Amianto et al., 2015).
Interestingly, those suffering from BED rarely exhibit long-term restrictive behaviors (i.e. multi-day fasts) but do often exhibit short-term restrictive behaviors (i.e. morning undereating) (Raymond et al., 2003). This speaks to a micro-pattern of “hedonic deprivation” in binge eaters that serves to continually reinforce the behavior by depriving themselves of rewarding sensations until a binge is inevitable (Lowe & Levine, 2005).
Not all individuals with BED suffer from it in the same way. At least one study has dichotomized sufferers into a purely dietary [binge eating] group and dietary-negative affect [binge eating] group (Carrard et al., 2012). It found the latter group was more anxious, engaged in more frequent and more intense binge behaviors, and had a greater sensitivity to punishment. This would all seem to imply treatment should be aimed at characterizing the level of negative affect in anyone suffering from BED, before then looking at treatment strategies: the purely dietary group does not merit the amount and intensity of emotion regulation exercises the dietary-negative affect group might.
The neurobiology of binge eating revolves around disturbances in dopaminergic and serotonergic pathways, as well as various endogenous opioids systems (Schag et al., 2013). As mentioned in What is Bulimia Nervosa?, BED’s neurobiological basis is separate from that of BN. Whereas BN presents with a hyperactive orbitofrontal cortex (OFC) and anterior cingulate cortex (ACC), as well as weakened inhibition from the lateral prefrontal circuits, BED shows alterations in the dorsal striatum and its eliciting of the reward-based food consumption in binge eating (Kessler et al., 2016).
The striatum is one of the most important subcortical structures in the brain. Located right in the center of the brain and oddly resembling a bluetooth piece, this is the hub for habit-based decision making and regulation. The dorsal striatum is the part that sends important signals to the basal ganglia, a collection of nuclei associated chiefly with voluntary movement and reward-seeking behaviors.
One study administered methylphenidate (generic Concerta, a stimulant often prescribed for attention deficit hyperactivity disorder, or ADHD) to obese individuals with and without BED (Wang et al., 2011). The BED group showed a dramatically altered dopamine response in the caudate nucleus, a structure within the dorsal striatum. As dopamine has long been understood to play a primary role in directing reward-based food intake (Bello & Hajnal, 2010), this could partially explain binge eating symptoms.
Literature reviews have highlighted the need to separate BED from other disturbed eating pattern pathologies, such as frequent snacking, emotional overeating, and selective cravings (Amianto et al., 2015).
If you’re wondering why we aren’t talking about sugar/food addiction, it’s because it was covered here:
READ: Is Sugar Addiction Real?
The dangers of BED are almost all also present in BN, but there are some that are not present in BN. This is because the weight loss and “mitigation” of binges that comes from compensatory behaviors (i.e. purging) renders the gastric side of things slightly less relevant. However, with BED, gastric retention of such large amounts of food can lead to significant health issues.
Literally speaking, gastric capacity will generally increase over time (Hellström et al., 2004). As well, the gastric pain experienced with severe binges can over time desensitize nociception cues (Raymond et al., 1995).
As the binge cycle serves to spur more and more of the very emotions that trigger binge eating, it can be hard to break the cycle and make a change. Binge eaters often feel trapped in this pattern of negative emotions leading to binge eating leading to body image issues leading to short-term restrictive behaviors leading to upregulated reward sensitivity leading to binge eating. Routine binge eating can also lead to (or worsen) social isolation behaviors (Leonidas & dos Santos, 2014).
So far the only FDA-approved drug for BED treatment is lisdexamfetamine (Vyvanse), a drug chiefly prescribed for ADHD (McElroy et al., 2015). There is concern that Vyvanse is habit-forming, and its stimulant properties mean it does not address behavioral patterns as much as it serves simply to blunt hunger and expedite weight loss.
Two more off-label drugs are commonly used to ameliorate symptoms: topiramate (Topamax) and antidepressants (primarily SSRIs). There is limited research on Topamax, and research on SSRI efficacy closely resembles the research for BN individuals.
It might be clear by now that pharmacological interventions do not offer what therapeutic ones do, especially when it comes to a disease like BED or BN. This has been proven in double-blind trials as well, where CBT not only beat out fluoxetine (a major SSRI) by large margins for every metric, but CBT alone also proved to be more effective than a combination of SSRIs and CBT (Grilo, Masheb & Wilson, 2005).
When it comes to psychotherapeutic approaches to BED treatment, just as with BN, cognitive behavioral therapy (CBT) remains the predominant mode of conventional therapy (Peterson et al., 2009). BN-specific CBT approaches are often used in BED treatment as well, as the binge event is the initial behavior we are targeting in either case (Iacovino et al., 2012). Rates of remission from CBT approaches alone hover around 60-70% (Castellini et al., 2011) at long-term follow up, proving this is the most effective treatment we currently have for BED. This is likely because it seeks to address root issues of the behaviors (Grilo et al., 2013), rather than just trying to break a habit loop alone.
Dialectical behavior therapy (DBT) is also frequently used in treating BED (Safer, Robinson & Jo, 2010). Where DBT shines is in its emphasis on emotion regulation and stress tolerance (Wiser & Telch, 1999), whereas CBT applies its focus purely to internal cognitive distortions. DBT boasts “abstinence” rates in the neighborhood of 50% by 6-month follow up, but there is markedly less research available on DBT interventions for BED than there is for CBT, so the evidence is not as robust.
Another common, albeit increasingly controversial, treatment is behavioral weight loss (BWL) (Grilo & Masheb, 2005). While BWL is able to provide weight loss, this is a surface-level symptom of BED and virtually unrelated to any causes, which could explain why CBT is so much more effective in properly run trials (Grilo et al., 2011).
Since prescription of weight loss regimens seems to be commonplace in cases of BED, it is important to look at the dangers in this and, on the flip side, the efficacy of the non-dieting approach. One of the landmark studies on the effects of a Health at Every Size (HAES)-based dietary intervention showed remission of binge eating symptoms (Ulian et al., 2015). Other trials using the HAES approach have similarly shown dramatic long-term reductions in disinhibition and eating in the absence of hunger (EAH) scores (Provencher et al., 2009).
A consistently effective predictor of remission from binge eating is early and rapid changes in behavior, during any intervention process (Nazar et al., 2017). This is the case for most eating disorders but might be especially true for BED (Iacovino et al., 2012).
Prognoses in BED vary, and these can be affected by psychological comorbidities like personality disorders (Amianto et al., 2011; Peterson et al., 2005). It is important that providers watch closely as BED patients move through the early stages of treatment. As mentioned earlier, different “subtypes” of BED exist, as this is a fundamentally “expressive” disorder, so interventions should be consistently tailored to maintain specificity and ensure expedient recovery (Wilson et al., 2010).
We can classify…
Partial remission as: After full criteria for BED were previously met, binge eating occurs at an average frequency of less than one episode per week for a sustained period of time.
Full remission as: After full criteria for BED were previously met, none of the criteria have been met for a sustained period of time.
NEDA - The largest national eating disorder advocacy forum, which regularly hosts outreach events, funds important research, and directly helps those affected via their helpline.
BEDA (Binge Eating Disorder Association) - This is another major outreach organization that serves to spread awareness of BED and provide help and fair access to health care for those who suffer from this disease.
AED (Academy for Eating Disorders) - Organization that specializes in ensuring the professional standards of eating disorder research, treatment, and information.
NEDA’s Helpline number is: 1-800-931-2237
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