Bingeing and Purging: Keeping the “Positives” and Eliminating The Negatives?

I have been fascinated and perplexed by reports of the seemingly invigorating and anxiety reducing effects of bingeing and purging (purging by self-induced vomiting). Personally, I cringe at the idea of self-induced vomiting and have always wanted to avoid vomiting at all costs, including during food poisoning. The insight from recent blog entries and the subsequent comments has made an impact on me. I see that the motivation to engage in bingeing/purging behavior can be intense and can provide an effective way increase positive affect and reduce stress. The ameliorating effects of bingeing/purging remind me of drug addiction, with bingeing/purging behavior as the “drug.”  This made me wonder, what happens in the brain to impart such “addiction-like” reinforcement?

I know there are reports of opiate and endorphin release following purging, but to me, this seemed like an effect meant to counter the intense aversion (and discomfort?) of the act of purging itself. Correct me if I’m wrong, but it seems like the feeling of being “empty” should be reinforcing as well. As someone who used to restrict quite a bit, I certainly found that feeling comforting and reinforcing. So, I wondered, was there any evidence that gastric emptying from bingeing/purging is reinforced in the way that drugs are reinforced: by increasing dopamine levels in the nucleus accumbens, a reward-related brain region that is involved in translating wants and needs into motivated action to seek rewards?

My search led me to this article  by Nicole Avena and colleagues. Dr. Avena is a renowned researcher who uses animal models to understand neurological changes associated with binge-eating behaviors. In this study, her lab used a rat model of bingeing behaviour (consuming a lot of sucrose) to look at the neurological effects of bingeing and purging on a 10% sucrose solution. Rats cannot vomit, so instead they used gastric fistulas, a tube-like structure implanted in the upper-portion of the stomach that can be opened to drain the contents of the stomach, to mimic purging. The fistulas were left open during the 1 hour of access to sucrose in the binge-purge rats, but not in the control rats that simply binged on sugar (without ‘purging’).


  • Over a period of 3 weeks, both groups enhanced their intake of sucrose during the access period.
  • Rats that had their stomach contents emptied always ate more and continued to eat for longer bouts of time than the controls.
  • Interestingly, dopamine responses within the nucleus accumbens did NOT differ between the two groups after this period:  both showed heightened levels of dopamine. This was thought to indicate that both groups had similar levels of motivation to binge eat.

If dopamine responses were the same, why did the animals with gastric fistulas eat more?

There can be dissociations between the motivation to seek out a reward and the actual consumption of that reward. Think about it this way: sometimes a drug addict will seek out their drug of choice, even when he/she no longer finds it all that enjoyable to take. Dopamine is thought to be primarily involved in “seeking” the reward–not in consuming it. Perhaps alterations in the levels of another neurotransmitter besides dopamine may be changing the way the body is interpreting the effects of consuming the food in the “binge-purge” rats?

Avena et al. found that levels of acetylcholine (another important neurotransmitter) in the nucleus accumbens were reduced in response to sucrose feeding in the gastric fistula (binge/purge) rats compared to the binge-eating controls. Enhanced acetylcholine levels in this brain region are thought to act as a “satiety signal” to decrease further food seeking and food consumption. If you block acetylcholine from acting on certain receptors in the nucleus accumbens with drugs that “mimic” the shape of the molecule, regular food intake patterns are disrupted (see article here). Interestingly, approach towards the food is not necessarily decreased, and sometimes elevated.

So, motivation for food was likely left intact, but without the feedback signal from acetylcholine (because it was reduced in response to sucrose in the binge/purge rats), the rats continued to binge (indeed, their bingeing increased over time.)

These results may reflect a simple dysregulation of acetylcholine signaling due to the lack of sensory feedback from the gut, but it may be something more.  In a review co-authored by Avena, the authors write that acetylcholine in the nucleus accumbens is also associated with avoidance behaviors in response to aversive stimuli, such as uncomfortable brain stimulation or bitter foods.

Could it be that gastric emptying by self-induced vomiting removes feelings of aversion and discomfort at a broad level (not just physiologically) and STILL leaves the invigorating effects of binge-food intake intact? Could the interplay of these two neurotransmitter systems contribute to escalating bingeing/purgingbehavior over time?


  1. In this model, bingeing/purging does not alter the motivation or impulse to binge on sugar, but rather makes the binge last longer.
  2. The progressive increase in bingeing may be due to alterations in acetylcholine due to “purging” the contents of the stomach.  This decrease in acetylcholine removes any aversive effects from binge food intake and is speculated to potentially alleviate aversion in other domains, like stressful/fearful situations that may be involved in initiating the binge behaviors themselves.

In other words, acetylcholine dysregulation (or reduction, as seen in the binge/purge rats) is speculated to reduce aversion for the short-term. And the lack of negative feedback from the act of binge eating is speculated to perpetuate engagement in binge eating as a source of “reinforcement” or escape.


Obviously, there are numerous differences between gastric emptying by fistulas and bingeing and purging in humans. For one, the gastric emptying is almost immediate in the rats, while individuals who bingeing/purging may not purge until several hours after they consume a food.

However, it is interesting that this neurochemical change is independent of any neurological effects due to the act of purging itself; the result is a correlate of gastric emptying. It would have been nice to see if the “purging” animals would WORK harder for their sucrose (e.g., requiring the animals to lever press for their sucrose). This would give a behavioral sign of whether these neurological correlates show an increased “drive” to engage in binge food intake.

Readers, do you think these studies may provide some insight into the intransigence of bingeing/purging behaviors?


Avena, N., Rada, P., Moise, N., & Hoebel, B. (2006). Sucrose sham feeding on a binge schedule releases accumbens dopamine repeatedly and eliminates the acetylcholine satiety response Neuroscience, 139 (3), 813-820 DOI: 10.1016/j.neuroscience.2005.12.037

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Liz received her PhD in Psychology at the University of Toronto. For her PhD, she used behavioral pharmacology techniques to study nicotine reinforcement. Liz is interested in the neurobiology of addictive/compulsive behaviours. She hopes to teach psychoeducation courses and empower individuals to take charge of their own recovery with enhanced knowledge of the inner workings of the brain.


  1. So interesting that this topic has come up again, as there was a similar discussion going on in the BHNDPG listserv. I also found these articles that discuss the different responses individuals have to the b/p cycle:
    – Luby ED & Koval D. CNS Opiate Systems and Eating Disorders.
    – Avena NM & Bocarsly ME. Dysregulation of brain reward systems in eating disorders: neurochemical information from animal models of binge eating, bulimia nervosa, and anorexia nervosa.
    – Jimerson DC & Wolfe BE. Neuropeptides in Eating Disorders.

    I always appreciate when the nitty-gritty of the neurochemical processes is broken down for me – so thank you!

    • Nice! I’m also a big fan of the Avena & Bocarsly review. I’ll have to check out the other two papers!

  2. “Obviously, there are numerous differences between gastric emptying by fistulas and bingeing and purging in humans. For one, the gastric emptying is almost immediate in the rats, while individuals who b/p may not purge until several hours after they consume a food.”

    I don’t think this is the main drawback of this study when it comes to the question of how relevant this is to humans. Removing the food by gastric emptying negates the whole /process/ of self-induced vomiting. Most people who binge/purge, purge immediately or shortly after (as far as I know), so I don’t think that’s a major problem. It is just that self-induced vomiting is a pretty labour intensive task whereas removing the food through the fistula isn’t. I don’t want to get into grotesque detail here, but it is hard for me to see the parallel (and I think those who purge through self-induced vomiting and have been for some time, know what I’m talking about).

    The empty feeling following a purge is nice, but to me, the act of self-induced vomiting is, in and of itself, a release. How do you mimic the pleasant light-headed feeling that comes after vomiting that I find so negatively reinforcing in a rat?

    I don’t have an intense aversion or discomfort when it comes to purging. I know some individuals with binge/purge AN or bulimia dislike it, but I know many who neither hate it nor like it, and others who enjoy it. So, I’m not convinced with the hypothesis endorphin release is to counter the negative aspects of the self-induced vomiting itself.

    It is really, really, important to remember that when it comes to the experience/feeling, self-induced vomiting is NOTHING like vomiting when you are sick. To me, having experienced both many times, I absolutely DETEST involuntary vomiting because of sickness. It is a terrible experience. Not so for self-induced vomiting, though.

    How do you think these findings relate to the reduction of blood sugar post-purge? Does that somehow relate to the acetylcholine findings? Because surely that’s a huge drive to binge/purge again, and binge more, too (since the blood sugar levels can drop to fasting levels).

    Is there anyway to measure these things in humans? Can we measure acetylcholine metabolites or something after purging? I’m just skeptical of the application of these findings to humans.

    Also–re your title: how do you suggest keeping the positives and eliminating the negatives?

    Great post, thanks Liz!


    • “It is really, really, important to remember that when it comes to the experience/feeling, self-induced vomiting is NOTHING like vomiting when you are sick. To me, having experienced both many times, I absolutely DETEST involuntary vomiting because of sickness. It is a terrible experience. Not so for self-induced vomiting, though.”

      Wow! Thanks so much for this. This is why I love hearing about actual experiences. I had NO idea that purging vs. vomiting while sick could be so different.

      I also agree with you that the process of bingeing and purging is an integral part of BP behavior in humans. What is interesting to me is that acetylcholine changes occur in the ABSENCE of performing this ritual, providing some evidence for a common alteration in brain chemistry that can occur regardless of variations in the behavioral process of bingeing in humans. That this change is exhibited in the absence of binge-purge behaviors and is correlated with binge length is interesting to me.

      In regards to the question about blood sugar, I think that’s a valid point! However, I’m not sure if it can completely explain the local changes of acetylcholine in the nucleus accumbens. Acetylcholine in this region does appear to increase with feeding and serve as a “satiety signal”, which should correlate with insulin release. Stimulating opiate receptors in the hypothalamus, which occurs when animals eat highly preferred foods, also lowers acetylcholine release in this area and encourages more intake of the preferred food. If it was simply associated with insulin, the acetylcholine levels should go down with consuming this food, which is usually high in sugar. So, maybe acetylcholine in the nucleus accumbens is some sort of “stop” signal for continuing to ingest foods and other sources of reinforcement (e.g. drugs)? Since increased ACh levels in the accumbens are also associated with aversive behaviors, perhaps it removes some sources of aversion? (really speculative)

      I haven’t seen anything with humans on acetylcholine levels in the nucleus accumbens after BP behaviors. My guess is we don’t have the radioligands to detect those changes in PET imaging studies…not to mention the complications that would surround BP and neuroimaging.

      So…keeping the “positives” I would argue to be the motivation to engage in the binge and perhaps the subjective pleasure of doing so. The “purge” may remove the “stop” signal, which may be something to do with satiety…or aversion…or a combination of both?

      • Hmmmm. . . OK so let me see if I understand this (I’m not familiar with the reward/addiction/DA literature – especially as it relates to b/p)

        The group that consumed more sucrose were those with the fistulas. Presumably these rats needed to consume more sucrose to compensate for the loss of sucrose via the fistula?

        Could the DA response be similar because the “seeking” behaviour is similar in both groups? (i.e. rats will preferentially administer a sucrose solution). . .

        If Ach acts as a satiety signal in the nucleus accumbens, it would be expected that there would be a reduction in satiety because these rats are not satiated in the same manner as the control group.

        I think the aversive behaviour angle is a bit of a stretch? (but maybe I am making a fool’s error because I am not familiar with the literature). . .

        Could it not be a more parsimonious explanation to suggest that the higher rate of consumption in the fistula group could be due to the loss of the actual hedonic “reward” response of the sucrose which could continue to reinforce consummatory behaviour?

        Ideally, it would be interesting to see a follow-up post on the neurochemistry of the aversion angle!

        • Also, this post made me wonder. . . what about just purging in the absence of binging?

          I find – at least for me – the anxiolytic effects of “just” purging are similar to what others report after a b/p – so is the binge component really necessary for this effect to be seen or is the effect simply driven by the purging action?

          As Tetyana pointed out – purging is fairly labour intensive and I would almost describe it as a method of self-harm (not to be graphic, but at least after a very thorough purge). . . I find that the after-effects are similar to what I would experience after self-harm. There is a light-headedness and dissociation type feeling that accompanies both behaviours – At least for me. . .

          I am not entirely familiar with the BN/AN-BP literature as I am with the AN-R literature, but it seems as though simply the act of purging (purging ANYTHING) is often neglected in research (after all, there are only two AN subtypes – AN-R and AN-BP).

          There seems to be great interest in the coupling of the b/p behaviours. . .

          Also, there are radioligands that at least bind to nicotinic receptors and are used in humans. . . At present they just suck. . .

        • “Could it not be a more parsimonious explanation to suggest that the higher rate of consumption in the fistula group could be due to the loss of the actual hedonic “reward” response of the sucrose which could continue to reinforce consummatory behaviour?” –> totally a reasonable explanation! Although, direct infusions of acetylcholine receptor agonists into the nucleus accumbens actually decreases food intake, without affecting “food seeking” (or behaviors directed at looking for/foraging for food, which is more associated with dopamine). However, it’s unclear whether those direct infusions really mimic the natural patterns of acetylcholine release that occur during regular feeding.

          And, yes, the similar DA response is thought to reflect similar “seeking” in both groups.

    • Great comment Tetyana. My experience with purging is that I do it to release emotions, be it anger or loneliness or overstimulation. I will drink water just so I can purge, or I will try to purge when I have not eaten anything. I binge to purge. Would love to see more on this topic.

  3. Great post! Thank you.

    I agree with Tetyana’s comments – with the questions she brought up.

    Another thought re self-induced vomiting – if the rats had to really work to eliminate the sucrose rather than have it eliminated for them via the fistula – would they? Many find purging pleasurable but just as many find it horrible – but do it anyway. What is it that drives people who hate it, to do it again?

    Personally, while I found my initial binges driven by extreme hunger, feelings of deprivation and/or high anxiety – if this became a string of binges rather than just one, it was usually because my blood sugar levels dropped enough to make me shaky and feel like I would pass out. In hospital, when I purged meals, my blood sugar levels crashed pretty soon afterwards, a couple of times to emergency levels.. I know for sure that if I was capable of bingeing again when I felt like this, I did it, despite not wanting to and being tired and weak.

    • Yeah, I wonder about the differences between bingeing/purging that results mostly from extreme hunger/starvation and those that occur when we are not really physically starving at all (but maybe are experiencing feelings we can’t tolerate OR are restricting specific foods, but not calorically overall).

    • Cool idea for a study, Fiona! I wonder if the rats would work to have their contents emptied as well.

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