BY: Andrew Hardaway, PhD

DATE: December 13, 2016

Binge eating disorder (BED) is now the most common eating disorder and, although it is fairly common (affecting about 3% of the population), there are only a few medications that clinicians can prescribe to treat BED (For a very thorough review of all BED behavioral or pharmacological treatments – see BED AHRQ report with contributions by CEED members Kim Brownley, Christine Peat, and Cynthia Bulik). Although new medications like lisdexamfetamine (Vyvanse) have been shown to be effective in general, they don’t work in ALL patients, nor do we know they work in the longer-term. Therefore, there is an emerging need to expand the range of medications either as solo treatments or for clinicians to pair with behavioral therapies.

SSRIs, serotonin selective reuptake inhibitors, have long been shown to reduce binge eating in both animal models and in the clinic, but a recent paper brings new clarity to the neural mechanisms by which these drugs bring about anti-binge effects. Serotonin is a brain neurotransmitter and body hormone that acts on several types of receptors – 14 of them! The serotonin 2c (5HT2C) receptor is expressed heavily throughout the brain, including areas of the brain that control feeding and reward. The authors of this paper nicely showed that fluoxetine (Prozac), an SSRI, reduces binge eating in mice and that this reduction happens via the actions of the 5HT2C receptor. Furthermore, they demonstrated that the brain’s serotonin and dopamine systems are interconnected and that the actions of the 5HT2C receptor in the brain’s dopamine reward system are required for binge eating behavior.

In 2012, the FDA approved lorcaserin (Belviq), a 5HT2C receptor activator, as a weight loss drug and for the treatment of type 2 diabetes. A number of important studies have shown that lorcaserin can activate neurons in the brain’s hypothalamus that reduce hunger, but its role in binge eating was unknown. Using genetically modified mice, the authors at Baylor College of Medicine nicely showed that lorcaserin can directly activate dopamine neurons in a reward center called the ventral tegmental area (VTA) and that this activation can suppress binge eating. They also demonstrated that activation of VTA dopamine neurons was necessary for the reduction in binge eating seen with serotonin releasing drugs.

This study is a proof-of-concept animal study that reveals an important potential therapeutic agent (lorcaserin) that might be “repurposed” for the treatment of BED. Considering the lengthy and expensive process of getting new drugs to the market, exploring lorcaserin’s clinical efficacy is a worthwhile effort to identify new medications to treat BED in the here and now.

That said, there are a number of important issues that might have to be addressed amongst BED patients and their care providers. Lorcaserin is a drug that is approved for weight loss, but for many individuals, weight loss is not considered to be a treatment goal. Rather they opt to focus on reduction or elimination of binge eating while developing greater acceptance of a range of body shapes and sizes and focusing on healthy lifestyles rather than weight loss. One other issue that needs to be monitored is that in animal models, high doses of lorcaserin can reduce general food consumption. If this also occurs in humans, it could be unintentionally disadvantageous for individuals with BED who are prone to binge when they experience longer periods of low food intake and low blood sugar. Careful evaluation of appropriate lorcaserin dosage for BED would need to be undertaken to avoid any “off-target” effects.

Right now, clinicians can choose from psychotherapies [e.g., cognitive-behavioral therapy (CBT), interpersonal psychotherapy (IPT)] and some medications (e.g., topirimate, lisdexamfetamine, and SSRIs) for the treatment of BED. But we know strikingly little about combining psychotherapies with medication and whether this produces superior and longer-term outcome. Even though many clinicians may use this approach in clinical practice, the outcome of “combination treatments” is one of the important research questions yet to be addressed.