What is Bulimia Nervosa?

Day 2 of National Eating Disorders Awareness Week is upon us, and today I have for you another comprehensive review. This time, we are taking a look at the second most well-known DSM-identified eating disorder: bulimia nervosa.

Definition and Diagnosis

Though bulimia nervosa (BN) is characterized most frequently by its “purging” (usually self-induced vomiting) component, the disease is a bit more complicated than what most might think.  As well, its interesting feedback pathology (binge/purge cycles) offer an opportunity to delve into some largely unexplored neurobiology and really learn something. Let’s dive into it.

To be diagnosed with BN, the DSM requires 5 qualifications:

  • Recurrent episodes of binge eating, which are characterized by both of the following:

    • Eating, in a discrete period of time, an amount of food larger than what most individuals would eat in a similar time frame under similar circumstances.

    • A sense of lost control over eating during the episode (feeling one cannot stop eating or control what or how much they are eating).

  • Recurrent inappropriate compensatory behaviors intended to prevent weight gain, including but not limited to:

    • Self-induced vomiting (by far the most common method)

    • Laxative abuse*

    • Diuretics

    • Fasting

    • Exercise

  • Binge-eating and compensatory behaviors occur an average of one or more times a week, for 3 months.

  • Self-evaluation is disproportionately influenced by one’s body weight and shape.

  • Disturbance does not occur exclusively during episodes of anorexia nervosa.**

*There is reason to believe abuse of laxatives represents a more severe BN pathology.

**This last bit of information points to the fact that nervous system deviations like anorexia and bulimia can occur in episodic fashion.  One can go from having bulimia to binge-eating or anorexia to bulimia, etc. (but it almost always occurs in the order of anorexia → bulimia → binge-eating, and rarely does it go in the other direction, bar episodic, subclinical occurrences).

Severity is ranked based on frequency of compensatory behaviors:

  • Mild: Average of 1-3 compensatory behaviors a week

  • Moderate: Average of 4-7 compensatory behaviors a week

  • Severe: Average of 8-13 compensatory behaviors a week

  • Extreme: Average of 14 or more compensatory behaviors a week

It is important to note that in the former DSM edition (DSM-IV), weekly binge frequency requirements for diagnosis were double what they are now (twice a week instead of once).  The reduced threshold was motivated by findings that many individuals reporting what would formerly be “subthreshold bulimia” were still experiencing subjectively equal amounts of distress and loss-of-control in their eating behaviors (Le Grange et al., 2004).  This suggests it is the subjective sensation of loss-of-control, rather than the objective amount of consumed food, that defines binge severity.

One interesting difference between the subjective experience of BN vs. AN in sufferers is that of psychoanalytics (Le Grange & Loeb, 2007).  Anorexia is considered to be experienced as ego-syntonic, meaning the manifestations of the illness feel “right” to the victim and their constructed identity (in other words, anorexics largely feel their behaviors are in line with who they are).  Bulimia, on the other hand, is ego-dystonic, meaning the behaviors and compulsions experienced are dissonant with the victim’s identity and ego (in other words, bulimics generally do not feel this is “them,” and almost feel possessed by some outside force).


All the way back to Ancient Greece, around the 300s BC, we have documented reports of Greek soldiers intentionally purging.  And in Rome, members of the elite class would sometimes purge themselves as a means of making room for more food. The term “bulimia” comes from the Greek boulīmia, which translates to “ravenous hunger.”

Interestingly to our discussion of individuals moving from one eating disorder to another, there are records of numerous saints whose anorexia (ostensibly set off by their ascetic livelihoods) turned into bulimia (or, at least, what we would now categorize as bulimic behaviors).  Regular binge-eating followed by a compensatory purging session was not unheard of in groups like this.

In 1979, Gerald Russell gave us the first published description of modern BN.  One year later, bulimia was introduced to the DSM-III. Since then, definitions have changed and medical diagnostic criteria altered, but the disease is still fundamentally understood to be the same one.


Between 1.1% and 4.6% of females, and between 0.1% and 0.5% of males, will develop BN at some point (Stice & Bohon, 2012). Those with BN are 1.5 times as likely to die of any cause than those without (Fichter & Quadflieg, 2016). BN very commonly exists alongside comorbid conditions, such as personality disorders or psychotic disorders, which can skew some of the long-term statistics we have.

Etiology and Pathophysiology

Risk factors more tightly attributed to BN pathology, versus AN, include family overeating, as the other common risk factor (sexual abuse) is shared among many psychiatric disorders.  Premorbid negative self-evaluation is also a disproportionately high risk factor (Fairburn et al., 1997). Genotypic variations tend to affect “intermediate phenotypes,” referencing factors like poor self-esteem and proclivity towards eating in the absence of hunger, rather than a broad, all-encompassing “bulimia phenotype” (Steiger & Bruce, 2007).

When it comes to the pathophysiology of BN, we are looking at two critical events: binge-eating and purging.  Interestingly, there seems to be a distinct neurobiological basis for the binge-eating patterns in BN from those found in BED.

With binge-eating disorder (BED), we see a dorsal striatum-based compulsive mode of reward-oriented food consumption (Kessler et al., 2016).  With BN, it is largely a hyperactive orbitofrontal cortex (OFC) and anterior cingulate cortex (ACC), alongside a weakened inhibitory signal from the lateral prefrontal circuits (Van den Eynde et al., 2010).  The OFC not only deals with higher-order cognitive processes, like executive decision-making, but also with sensory processing (specifically flavor and smell), via limbic connections (Small et al., 2007).  This provides insights into the connections between taste and appetite dysregulation in BN patients and maladaptive cognitive processes.  

The ACC, on the other hand, has different limbic connections worth noting. It communicates with the amygdala and hypothalamus and might have implications for how we connect emotion to external stimuli in our environment (Etkin, Egner & Kalisch, 2011).  For these two areas to be hyperactive in BN provides evidence for where the maladaptations are occurring.  

Finally, the lateral prefrontal cortex adds another piece to this puzzle.  Boasting more recent discoveries than the OFC or ACC, this circuit is said to play a role in “behavioral planning,” ideally ensuring behaviors are in line with long-term judgment.  For this to elicit weakened inhibitory signals in BN patients would make sense, as it would remove some of the executive judgment involved in weighing out rewards and risks of binge/purge (b/p) behaviors (Tanji & Hoshi, 2008). And there’s no question decreased activation of executive control networks, more holistically speaking, is at play in the BN pathology (Seitz et al., 2016).

Unfortunately, there is still markedly limited research into the neurobiology of purging behaviors, despite an abundance of research into the basis of binge-eating and eating in the absence of hunger.  However, there are some insights worth noting:

  • Currently, the affect regulation model of BN is the most widely accepted.  It posits that cyclical binge and purge patterns exist solely to mitigate negative affective states (Berg et al., 2013).

    • An extrapolation of this theory is that guilt is the predominant regulatory emotion in BN, as it has shown to be the most consistently reported facet of negative affect during bulimic episodes and shows the most linear relationship with b/p mediation (i.e. its consistency in being high before b/p behaviors and low after is unparalleled by other forms of negative affect, such as anger or sadness).

  • Animal research suggests purging reduces the release of the neurotransmitter acetylcholine, which is correlated with aversive states (such as drug withdrawal) (Avena et al., 2006).

  • Apomorphine, a dopamine promoter commonly used in acute dopamine challenge tests in studies, has been shown to elicit extreme nausea and vomiting only in anorexic and bulimic patients, with no response seen in healthy controls (Bello & Hajnal, 2010).

    • Where this becomes interesting to us is the fact that hindbrain “chemoreceptor trigger zone” (CTZ) sites, which are chiefly responsible for stimulating the vomit response, contain dopamine receptors.  This finding might indicate that the dopamine receptors in this region are more sensitive in those with a pathological inclination to purging behaviors (i.e. anorexia purge type, bulimia nervosa, purging disorder, and potentially rumination).

    • And since the major neurotransmitters involved in the CTZ-initiated emetic (vomiting) response are serotonin and dopamine (Linklater, 2014), it makes sense that these neurotransmitters are consistently shown to be dysregulated in AN and BN (Bailer & Kaye, 2011).

Unlike AN, there is limited to no evidence for a microbial or evolutionary basis to the pathology of BN.  However, this disease has not received the same amount of academic attention and is admittedly often lumped into studies meant primarily to look at AN-specific symptoms.


The self-induced vomiting component of traditional bulimic behaviors carries its own array of health risks, including:

  • Thickened skin on the knuckles

  • Worn down enamels (not only from the hydrochloric acid in the vomitus but the constant abrasive interaction of the hand with the backs of the teeth)

Purging via vomiting or laxative/diuretic abuse poses an especially great risk of electrolyte depletion.  This can easily lead to sudden cardiac or respiratory failure, as these electrolytes all play a vital role in basic metabolic functions, and osmotic dysregulation can precipitate a whole chain of nasty events.  

See the picture below for a comprehensive look at the multiple body areas bulimia will affect:



Selective serotonin reuptake-inhibitors (SSRIs) might be effective in mitigating some of the symptoms in BN, but it’s worth noting participants who have taken these antidepressants had a higher rate of dropout during clinical trials, usually due to adverse effects of the medication (Bacaltchuk & Hay, 2003). Fluoxetine, which is currently the only SSRI approved by the FDA for the treatment of BN, has empirical backing for its usage in treating BN, and it has a dose-response relationship with BN symptoms (FBNCSG, 1992).

SSRIs, or any medication for that matter, should only serve to allow for a more appropriate serotonin/dopamine response.  When these medications are used to blunt hunger or even induce weight loss, there is risk of ignoring the root of the issue in favor of surface-level “results,” which could spiral the individual back into relapse.  

Also worthy of note, whether a patient will be a non-responder or not can usually be identified early in the course of SSRI treatment, so if symptoms are not subsiding by approximately the third week, he or she will likely need other modes of treatment instead* (Sysko et al., 2010).

*This is not medical guidance, and ultimately a medical provider should make this call.

When it comes to therapeutic models applied to BN treatment, cognitive behavioral therapy (CBT) is unanimously seen as the number one option (The National Institute for Health Care and Excellence).  Though multiple reviews have shown objective metrics of improved recovery in BN patients who underwent CBT trials (Shapiro et al., 2007; Hay et al., 2009), there is reason to believe it can still stand to be improved.  In fact, CBT treatment in its purest form can only boast less than 50% rates of full recovery (Wilson, Grilo & Vitousek, 2007).

To this end, Fairburn, Cooper, and Shafran (2008) devised what is known as “enhanced CBT” for eating disorder psychopathology specifically.  Where it deviates from standard CBT models is in its use of modules to address ED-specific obstacles, such as low self-esteem, perfectionism, and interpersonal deficits.  This is still being studied and perfected.

When comparing CBT and pharmacological interventions, numerous statistically significant study findings tell us that there is little or no difference, as it pertains to frequency of b/p events by the end of treatment (British Psychological Society).


One of the most consistently reliable predictors of therapeutic outcome is frequency of b/p episodes (Skunde et al., 2016).  While this might sound painfully obvious, it tells us that this outward symptom cannot afford to be ignored or minimized.  A patient who seems to be “subjectively recovered” in all realms other than b/p frequency should lull practitioners into a false sense of security, as these symptoms are an unavoidably paramount marker of remission.

A few factors disproportionately affect prognosis.  Correlated with positive prognoses are factors such as shorter duration of illness, higher social class, and younger age of disease onset.  Correlated with negative prognoses are factors like substance abuse history and comorbid personality disorder (Hay & Claudino, 2010).

One more important predictor of positive outcome is being in the right stage of change (Wolk & Devlin, 2001).  This originates from the transtheoretical model, which posits there are six stages of change all people go through: precontemplation, contemplation, preparation, action, maintenance, and termination.  Being in the “right” stage of change generally means being past the contemplation phase.

We can classify…

  • Partial remission as: Not all criteria of BN have been met for a discrete period of time.

  • Full remission as: None of the criteria of BN have been met for a discrete 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.

  • ANAD (National Association of Anorexia and Related Disorders) - Non-profit corporation that advocates for and seeks to spread awareness of eating disorders, especially anorexia nervosa and bulimia nervosa.

  • 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


  1. Avena NM, Rada P, Moise N, Hoebel BG. Sucrose sham feeding on a binge schedule releases accumbens dopamine repeatedly and eliminates the acetylcholine satiety response. Neuroscience 139: 813–820, 2006.

  2. Bacaltchuk J, Hay P. Antidepressants versus placebo for people with bulimia nervosa. Cochrane Database Syst Rev : CD003391, 2003.

  3. Bailer UF, Kaye WH. Serotonin: Imaging Findings in Eating Disorders. Curr Top Behav Neurosci 6: 59–79, 2011.

  4. Bello NT, Hajnal A. Dopamine and binge eating behaviors. Pharmacol Biochem Behav 97: 25–33, 2010.

  5. Berg KC, Crosby RD, Cao L, Peterson CB, Engel SG, Mitchell JE, Wonderlich SA. Facets of Negative Affect Prior to and Following Binge-Only, Purge-Only, and Binge/Purge Events in Women With Bulimia Nervosa. J Abnorm Psychol 122: 111–118, 2013.

  6. Etkin A, Egner T, Kalisch R. Emotional processing in anterior cingulate and medial prefrontal cortex. Trends Cogn Sci 15: 85–93, 2011.

  7. Fairburn CG, Welch SL, Doll HA, Davies BA, O’Connor ME. Risk factors for bulimia nervosa. A community-based case-control study. Arch Gen Psychiatry 54: 509–517, 1997.

  8. Fairburn CG, Cooper Z, Shafran R. Enhanced cognitive behavior therapy for eating disorders (“CBT-E”): an overview. In: Fairburn CG, editor. Cognitive Behavior Therapy and Eating Disorders. Guilford; New York: 2008.

  9. Fichter MM, Quadflieg N. Mortality in eating disorders - results of a large prospective clinical longitudinal study. International Journal of Eating Disorders 49: 391–401, 2016.

  10. Fluoxetine Bulimia Nervosa Collaborative Study Group. Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo-controlled, double-blind trial. Arch Gen Psychiatry 49: 139–147, 1992.

  11. Hay PJ, Claudino AM. Bulimia nervosa [Online]. BMJ Clin Evid 2010, 2010. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3275326/ [26 Feb. 2019].

  12. Hay PP, Bacaltchuk J, Stefano S, Kashyap P. Psychological treatments for bulimia nervosa and binging. Cochrane Database Syst Rev : CD000562, 2009.

  13. Health (UK) NCC. Treatment and management of bulimia nervosa [Online]. British Psychological Society (UK). https://www.ncbi.nlm.nih.gov/books/NBK49308/ [26 Feb. 2019].

  14. Kessler RM, Hutson PH, Herman BK, Potenza MN. The neurobiological basis of binge-eating disorder. Neurosci Biobehav Rev 63: 223–238, 2016.

  15. Le Grange D, Loeb KL. Early identification and treatment of eating disorders: prodrome to syndrome. Early Interv Psychiatry 1: 27–39, 2007.

  16. Le Grange D, Loeb KL, Van Orman S, Jellar CC. Bulimia nervosa in adolescents: a disorder in evolution? Arch Pediatr Adolesc Med 158: 478–482, 2004.

  17. Linklater G. Nausea and vomiting. The Journal of the Royal College of Physicians of Edinburgh 44: 218–223, 2014.

  18. Seitz J, Hueck M, Dahmen B, Schulte-Rüther M, Legenbauer T, Herpertz-Dahlmann B, Konrad K. Attention Network Dysfunction in Bulimia Nervosa - An fMRI Study. PLoS ONE 11: e0161329, 2016.

  19. Shapiro JR, Berkman ND, Brownley KA, Sedway JA, Lohr KN, Bulik CM. Bulimia nervosa treatment: a systematic review of randomized controlled trials. Int J Eat Disord 40: 321–336, 2007.

  20. Skunde M, Walther S, Simon JJ, Wu M, Bendszus M, Herzog W, Friederich H-C. Neural signature of behavioural inhibition in women with bulimia nervosa. J Psychiatry Neurosci 41: E69-78, 2016.

  21. Small DM, Bender G, Veldhuizen MG, Rudenga K, Nachtigal D, Felsted J. The role of the human orbitofrontal cortex in taste and flavor processing. Ann N Y Acad Sci 1121: 136–151, 2007.

  22. Steiger H, Bruce KR. Phenotypes, endophenotypes, and genotypes in bulimia spectrum eating disorders. Can J Psychiatry 52: 220–227, 2007.

  23. Stice E, Bohon C. Eating Disorders. In Child and Adolescent Psychopathology, 2nd Edition, Theodore Beauchaine & Stephen Linshaw, eds. New York: Wiley. (2012).

  24. Sysko R, Sha N, Wang Y, Duan N, Walsh BT. Early Response to Antidepressant Treatment in Bulimia Nervosa. Psychol Med 40, 2010.

  25. Tanji J, Hoshi E. Role of the Lateral Prefrontal Cortex in Executive Behavioral Control. Physiological Reviews 88: 37–57, 2008.

  26. Van den Eynde F, Claudino AM, Mogg A, Horrell L, Stahl D, Ribeiro W, Uher R, Campbell I, Schmidt U. Repetitive transcranial magnetic stimulation reduces cue-induced food craving in bulimic disorders. Biol Psychiatry 67: 793–795, 2010.

  27. Wilson GT, Grilo CM, Vitousek KM. Psychological treatment of eating disorders. Am Psychol 62: 199–216, 2007.

  28. Wolk SL, Devlin MJ. Stage of change as a predictor of response to psychotherapy for bulimia nervosa. Int J Eat Disord 30: 96–100, 2001.

  29. NICE | The National Institute for Health and Care Excellence [Online]. NICE: [date unknown]. https://www.nice.org.uk/ [26 Feb. 2019].