This is another post in Sci’s investigation into the current studies being performed on eating disorders, particularly binge eating and bulimia. Usually I try to focus on the dysregulation of reward-related systems in these disorders, but this paper will be a little different.
Faris et al. “De-Stabilization of the Positive Vago-Vagal Reflex in Bulimia Nervosa” Physiology and Behavior, 2008.
It’s kind of in the nature of an eating disorder that there aren’t any really funny pictures or something that Sci can put in here.
So before we go forward, here’s a kitten.
All right. So as you might be aware, bulimia nervosa is an eating disorder characterized by two stages, bingeing and purging. Bingeing, in this case, is total loss of control over the amount you eat (or even WHAT you eat, bulimics will eat raw eggs if they aren’t out of the way) during an episode. The patient then goes through a purge, which most people usually think of as vomiting, but which can also include misuse of things like laxatives, excessive exercise, and fasting. Bulimia nervosa is also characterized by body dysmorphia, the feeling that your body is intensely unattractive and overweight, regardless of evidence to the contrary. Often bulimics will start out purging in an effort to control their caloric intake, and binging and purging will then steadily become an obsession and a compulsion. Bulimia is thought to affect 3% of the female population (the vast majority of bulimics are female, though some males do exhibit bulimia) and up to 6% of the college female population.
Now, bulimia can be deadly if it goes far enough. It doesn’t have the mortality rate of anorexia, but it does have long term medical consequences associated with it (in the case of purging, for example, vomiting is terrible for your tooth enamel, not to mention problems with gastric reflux. Bulimics also can end up with major metabolism problems). So, you might ask, how do we go about treating it?
Well…that’s the thing. We don’t really. Well, ok, we DO, but very little is understood about bulimia and thus the treatments are not really understood either. Many bulimics do well with cognitive behavioral therapy and group therapy. For drugs, the big one approved for treatment of bulimia right now is fluoxetine, or Prozac. No one really knows why, but serotonin reuptake inhibitors appear to work in about 50% of bulimics, regardless of whether or not they are depressed.
But what about the other 50%? What about the people who don’t respond to these drugs? Well, scientists are still out to find an answer.
And this paper has a rather new hypothesis: the vagus nerve is to blame.
What’s the vagus nerve? Otherwise known as cranial nerve ten, the vagus nerve hits a whole bunch of stuff as it heads downward from the brainstem. It’s known to affect heart rate, breathing, the larynx, swallowing, and parts of digestion (including peristalsis, which is the moving of food, and the release of bile from the liver). Because of all of this, and especially the gastrointestinal stuff, it’s thought that stimulation of the vagus nerve may have something to do with feeding, specifically meal portion size and feelings of satisfaction after a meal. And this might have something to do with bulimia. Bulimics show consistent problems estimating meal size and satiety following eating (though really, given restaurant portions, who can estimate that these days). Not only that, feelings of satiety and control of vomiting have commonalities in neurotransmission.
However, what’s really important is that bulimics show abnormal responses to stimulation of the vagus on satiety and emesis, compared to controls (which you might expect after rounds of bingeing and purging). Not only that, bulimics also show different different responses to vagal-mediated pain sensitivity, which appear to show that their vagus is less sensitive.
Above you can see a graph showing the sensitivity to pain in the fingers of bulimic patients vs controls. You can see that controls (dark grey) had lower pain thresholds (felt the pain sooner) than bulimic patients.
Based on these and other findings, the authors of this study hypothesized that over stimulation of the vagus during the binge and purge cycles of bulimia results in a “dysregulated” (that’s their word, Sci would say less sensitive) vagus. Constantly stimulating the vagus via overeating, and then stimulating again via purging, might end up making the vagus less sensitive.
Up there you can see a correlation in bulimic patients between the time since the last binge/purge episode and the sensitivity to pain. You can see that sensitivity to pain appears to decrease as the time since the last binge increases, showing that there may be desensitization of pain sensitivity between binges.
So, if people with bulimia have reduced vagal sensitivity, you might be able to break the cycle by changing vagal sensitivity in between binges. To test this, the authors gave ondansetron, a serotonin 3 receptor agonist which reduces the activity of the vagus nerve. The idea (as far as Sci can tell), is that vagal activity is too over stimulated in these patients. When they give ondansetron, they shut down the vagus nerve and decrease vomiting. And they got this:
You can see that ondansetron treatment decreased the number of binge/purge episodes per week, and increased the number of normal meals. It looks like stopping the vomiting (ondansetron is a powerful antiemetic) helps to break the binge/purge cycle. They also found that stimulating the vagus nerve over time in these patients helped them eat more normal meals and feel more satisfied after them.
To bring it all together, the authors propose a model that, while normal people have a normal linear response to food intake (ranging from hungry to OMG full), bulimic patients have an oscillating pattern of response. They go from being unable to stop themselves from binge eating to being unable to detect when they are full, triggering a vomiting episode, like this;
They go on to say that new directions for research might be had in stopping the cycle with drugs that either increase feelings of satiety or stop vomiting in bulimic patients.
Sci thinks this model may have some merit. Certainly, if the patient can’t vomit, they won’t be able to binge as much, and breaking the cycle in such a way may be a good start for other kinds of therapy to take over. But I’m concerned about what will happen when you go off the drugs, and suddenly may be more sensitive to the vomiting reflex. Will the cycle start over?
In addition, while this controls the symptoms and the results of long-term bingeing and purging, this model doesn’t really contend with WHY people begin, and continue, this activity in the first place. So it treats the symptoms of bulimia, but may not affect the underlying cause. It certainly doesn’t affect the body dysmorphia that bulimia patients have, and the authors did not look at the URGE to binge and purge, only the results (also this was in a treatment population which will have issues of its own in that regard).
In the end, this model may not be the be all behind bulimia. In fact, it’s certainly not. But it may, as the authors suggest, help to find ways to stop the cycle of bingeing and purging long enough to try other methods of treatment, and long enough to stop some major health consequences before they become fatal. It’s not enough, but it may be a start.
FARIS, P., HOFBAUER, R., DAUGHTERS, R., VANDENLANGENBERG, E., IVERSEN, L., GOODALE, R., MAXWELL, R., ECKERT, E., & HARTMAN, B. (2008). De-stabilization of the positive vago-vagal reflex in bulimia nervosa Physiology & Behavior, 94 (1), 136-153 DOI: 10.1016/j.physbeh.2007.11.036