Investigational Pharmacological Treatments for Bulimia Nervosa

Current Research Updates from King’s College London

Bulimia nervosa is a serious psychiatric disorder characterized by recurrent loss-of-control binge eating, which is followed by excessive compensatory behaviors. With a 68.2% recovery rate at 9-year follow-up, bulimia nervosa is associated with a greater chance of recovery than anorexia nervosa. Even so, recent research has found that over 30% of individuals with bulimia do not recover over a 22-year time span, and as many as 50% of individuals do not respond to cognitive-behavioral therapy.

Researchers at King’s College London, and elsewhere, therefore continue to explore novel treatments that would promote remission among the individuals who do not respond to currently available treatments. Although medication should not be the first line of treatment, or sole treatment, for bulimia nervosa, in some cases medication can complement and enhance the benefits yielded by psychological interventions alone.

It has, for example, been found that adding an antidepressant to cognitive-behavioral therapy can help to reduce the frequency of purging. However, new pharmacological approaches are currently being investigated that aim to target other processes that maintain the binge-purge cycle.


Oxytocin is a naturally-occurring hormone in the body, which may be dysregulated or expressed differently in women with binge-purge tendencies. In addition to its role in modulating social cognition and behaviors, oxytocin has also been found to have effects on eating, as well as addictive tendencies in animals. Preliminary research in humans has demonstrated that oxytocin can reduce subsequent feeding, with a greater effect for hedonic, as opposed to hunger-driven, eating.

Furthermore, one study so far has already shown that a single dose of an intranasal spray oxytocin can reduce feeding so that it draws closer to the adult daily average intake in individuals with bulimia nervosa. Although preliminary, these initial findings are promising, and highlight the possibility that intranasal oxytocin may be a useful supplement to prevent loss-of-control binge eating amongst individuals with bulimia nervosa.

It is not yet certain how oxytocin acts to suppress feeding, but may involve a combination of influencing hunger centers, as well as reward centers, in the brain. Current research at King’s College London is expanding our knowledge of oxytocin’s effects in eating disorders, by further scrutinizing whether oxytocin does indeed normalize eating in bulimia nervosa and binge eating disorder. This research also aims to identify oxytocin’s mechanism of action in humans through the use of functional MRI scans, which will specifically examine how oxytocin impacts brain activity while participants experience different tastes.

Although we are a long way from being able to prescribe oxytocin as a proven supplement to psychological therapy in bulimia nervosa and binge eating disorder, these initial research studies have been very exciting for the field, and may pave the way towards more robust randomized controlled trials in the future.


In addition to investigating the effects of oxytocin, researchers have looked into the possibility of more directly intervening with reward- and addiction-related pathways. The concept of referring to recurrent binge eating as a “food addiction” is highly controversial within the field and the lay public, largely for the social, and sometimes stigmatized, implications that the term “addiction” carries. However, at a neuronal level we do know that opioid receptors in the brain (which are involved with processing reward) develop greater tolerance when an individual engages in habitual binge eating. This results in the opioid receptors losing sensitivity over time, in a similar fashion to that which occurs in response to repeated substance use. This desensitization then increases the likelihood that greater levels of binging will occur in the future, in order to achieve the same initial reward response. This cycle promotes the binging to become a more ingrained behavior.

Naloxone is a type of chemical known as an “opioid antagonist”. This means that it binds to the same receptors that opioids do. Instead of activating these neurons, however, naloxone simply blocks off the receptors so that opioids cannot act on them. Naloxone is therefore commonly administered when an individual has an opioid overdose, because it blocks the potentially deadly action that could be triggered by an excessive amount of opioids within the body.

In addition to this life-saving effect in emergencies, researchers have found that chronic small doses of intranasal naloxone can be useful to assist individuals who are recovering from substance dependence, such as alcoholism. Using an intranasal spray of naloxone helps to prevent the reward triggered by a substance. Therefore naloxone is believed to promote the cessation (technically known as “extinction”) of a behavior by blocking the rewarding aspect of it. From a neurobiological level, naloxone administration prevents the desensitization of opioid receptors, and supports their return to normal functioning.

Although recurrent alcohol addiction and recurrent loss-of-control binge eating differ in many important ways, there are some common neural pathways that keep both disorders going. This gives eating disorder researchers reason to believe that it may be helpful to investigate treatments that target these common pathways. Indeed, studies have already found that another opioid antagonist, naltrexone, may reduce symptoms of bulimia nervosa, including the duration of binge eating.

A clinical trial testing the effectiveness of intranasal naloxone in reducing binge eating in bulimia nervosa is currently underway in the United Kingdom. Although results are not yet available, researchers are hopeful that naloxone, oxytocin, and/or other treatments being investigated will ultimately prove to promote recovery from bulimia nervosa. Research into effective treatments has come a long way since bulimia nervosa was first described in 1979, and it is hoped that these latest investigations, as well as other intervention research in the field, will bring the field of eating disorders research one step closer to being able to support recovery for every affected individual.


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1. Eddy, K.T., et al., Recovery From Anorexia Nervosa and Bulimia Nervosa at 22-Year Follow-Up. The Journal of clinical psychiatry, 2017. 78(2): p. 184-189.
2. Poulsen, S., et al., A randomized controlled trial of psychoanalytic psychotherapy or cognitive-behavioral therapy for bulimia nervosa. American Journal of Psychiatry, 2014. 171(1): p. 109-116.
3. National Institute for Health and Clinical Excellence, Eating Disorders: recognition and treatment. NICE Guideline (NG69), 2017.
4. Acevedo, S.F., et al., Severity of eating disorder symptoms related to oxytocin receptor polymorphisms in anorexia nervosa. Psychiatry Res, 2015. 228(3): p. 641-8.
5. Bartz, J.A., et al., Social effects of oxytocin in humans: context and person matter. Trends in cognitive sciences, 2011. 15(7): p. 301-309.
6. Olszewski, P., A. Klockars, and A. Levine, Oxytocin: A conditional anorexigen whose effects on appetite depend on the physiological, behavioral and social contexts. Journal of Neuroendocrinology, 2016. 28(4): p. No Pagination Specified.
7. Sarnyai, Z. and G.L. Kovács, Oxytocin in learning and addiction: from early discoveries to the present. Pharmacology Biochemistry and Behavior, 2014. 119: p. 3-9.
8. Thienel, M., et al., Oxytocin’s inhibitory effect on food intake is stronger in obese than normal-weight men. International Journal of Obesity November, 2016. 40(11): p. 1707-1714.
9. Kim, Y., et al., The impact of oxytocin on food intake and emotion recognition in patients with eating disorders: a double-blind single dose within-subject cross-over design. PLoS ONE, 2015. 10(9).
10. Klockars, A., et al., Intravenous administration of oxytocin in rats acutely decreases deprivation-induced chow intake, but it fails to affect consumption of palatable solutions. Peptides, 2017. 93: p. 13-19.
11. Colantuoni, C., et al., Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence. Obesity, 2002. 10(6): p. 478-488.
12. Colantuoni, C., et al., Excessive sugar intake alters binding to dopamine and mu-opioid receptors in the brain. Neuroreport, 2001. 12(16): p. 3549-3552.
13. Doe-Simkins, M., et al., Saved by the nose: bystander-administered intranasal naloxone hydrochloride for opioid overdose. American Journal of Public Health, 2009. 99(5): p. 788-791.
14. Sinclair, J.D., H. Scheinin, and R. Lammintausta, Repetitive administration prior to drinking; opiate antagonist. 1992, Google Patents.
15. Flavell, C.R., D.J. Barber, and J.L. Lee, Behavioural memory reconsolidation of food and fear memories. Nature communications, 2011. 2: p. 504.
16. Jonas, J. and M. Gold, Naltrexone reverses bulimic symptoms. The Lancet, 1986. 327(8484): p. 807.
17. Alger, S.A., et al., Effect of a tricyclic antidepressant and opiate antagonist on binge-eating behavior in normoweight bulimic and obese, binge-eating subjects. The American journal of clinical nutrition, 1991. 53(4): p. 865-871.
18. Russell, G., Bulimia nervosa: an ominous variant of anorexia nervosa. Psychological medicine, 1979. 9(3): p. 429-448.

About the Author:

Monica Leslie is a PhD Candidate at the Institute of Psychiatry, Psychology, and Neuroscience within King’s College London. She holds a Bachelor of Science degree with Honors from The University of Western Australia, where she investigated the relationship between obsessionality and eating disorder symptoms in anorexia nervosa. Her current research focuses on the development of novel pharmacological approaches for binge-type eating disorders, which she studies under the supervision of Professor Janet Treasure. Follow this link to find out more about other research taking place at King’s College London.

Written – 2017