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’).
SUMMARY OF MAIN FINDINGS:
- 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?
TO SUMMARIZE THE FINDINGS
- In this model, bingeing/purging does not alter the motivation or impulse to binge on sugar, but rather makes the binge last longer.
- 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