In 1967, Routtenberg and Kuznesof reported a very peculiar phenomenon in rats:
They discovered that when rats were on a restricted feeding schedule (1 hour per day in their experiment) and had free access to a running wheel, their food intake was significantly lower than in control rats, which were on the same feeding schedule but without access to a running wheel. This discrepancy between increased running activity and decreased food intake caused substantial body weight loss, and if rats were not removed from the experimental setup timely, they would eventually die of starvation. This model, later named the activity-based anorexia (ABA) model, is one of the most widely used animal models for the study of anorexia nervosa (AN). (Source)
Of course, rats are not humans. Nonetheless, animal models of anorexia nervosa can inform us of some of the underlying neuropsychological and physiological influences and consequences of anorexia nervosa.They can help us understand what leads to and happens as a result of self-induced weight loss, restriction, and hyperactivity.
The benefit of using the ABA model (all …
What is different about anorexia nervosa sufferers that, in contrast to most dieters, enables them to maintain a persistent calorie deficit? Although no one can truthfully claim they know the full answer to that question, we do know that part of the answer most likely lies with serotonin (5-HT), a molecule that neurons use to communicate with each other.
I’ve written about serotonin in the context of anorexia nervosa before, so I’ll just do a brief summary of the important points here:
Given that serotonin mediates a lot of psychological and physiological traits associated with …
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 (b/p-ing) behavior can be intense and can provide an effective way increase positive affect and reduce stress. The ameliorating effects of b/p-ing remind me of drug addiction, with b/p-ing 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 …
The recent New York City soda ban controversy has contributed to increased discussion about the “addictive” properties of sugar and its contribution to the obesity epidemic. While I do not deny that there is an overabundance of high-sugar/high-fat foods in the societal milieu, and that the rewarding properties of these foods encourages their overconsumption; I think it is a mischaracterization to refer to the typical overeating associated with the “obesity epidemic” as reflective of a widespread “sugar addiction” that millions have fallen prey to.
Stice, Figlewicz, Gosnell, Levine, and Pratt (2012) have recently released a review in Neuroscience and Biobehavioral Reviews entitled “The contribution of brain reward circuits to the obesity epidemic.” In the paper, the authors elegantly describe the overlap between food and drug rewards while also highlighting major differences.
BRIEF INTRO TO DOPAMINE SIGNALLING
Before discussing the parallels between food and drug rewards, we should first introduce some of the neurological correlates of reward processing in general. All stimuli of motivational significance elicit dopamine release in a subcortical region called the nucleus accumbens.
These stimuli can range from …
This is part IV in my mini-series on the role of dopamine in anorexia nervosa. In part I, I did a a little introduction on dopamine and dopamine signalling in the brain. In part II, I discussed preclinical studies using animal models to study the role of dopamine in AN. Finally, in part III, I talked about clinical studies using patients with AN to assess dopamine function. In this final post, I’ll review the evidence for using drugs that modulate the dopamine system in order to treat anorexia nervosa.
It is going to be short, because there’s really not that much evidence that any pharmacological agents help in treating anorexia nervosa. To quote the authors of this review study,
No single psychological intervention has shown clear superiority in treating adults with AN.
… the first line of treatment for underweight patients with AN should be refeeding and weight restoration. This could be accomplished in a structured eating disorders treatment program without the use of medication (Barbarich et al., 2003).
However, in the last two posts, I provided some evidence suggesting …
This is part III of my series on the role of dopamine in anorexia nervosa. In my first post I did a little introduction on dopamine and dopaminergic signalling. In the second post I talked about preclinical studies that used animal models of anorexia nervosa. In this post I’ll briefly go over some of the research that has used patients with anorexia nervosa to understand the role of dopamine in this disorder.
I’ve got to be honest here: I wish things were simpler. I wish the research wasn’t so contradictory–but it often is. When you first start to explore a topic, and you are not even sure you are asking exactly the right question, things often look messy. I find this is true for my own research as well, and as a graduate student, it is hard to accept contradictory results. Yet, it is also hard as a science blogger to write about contradictory findings because it can be confusing, and messy.
But, stay with me. I’ll try to make it as simple as possible.
In the last post I …
This is part II in my series of posts on the role of dopamine in anorexia nervosa. (You can find the first part, which covers the basics of dopamine signalling, here.) In this post I’m going to discuss the findings from preclinical studies (studies in animal models).
I don’t think I’ve talked about animal models of anorexia nervosa before on the blog, but believe or not, they exist. The most well-known one is called activity-based anorexia (ABA). ABA works like this: rats are simultaneously restricted in the amount of food they can eat and given access to a running wheel. As the rats experience a reduction in their caloric intake, they begin to spend more and more time running on the wheel. A similar model with basically the same premise is called starvation-induced hyperactivity. These models are thought to mimic both the restriction/weight-loss and excessive exercise components of anorexia nervosa.
The ABA model has been used to study various aspects of anorexia nervosa, including the relationship between AN and over-exercise. Given that dopamine is known to be involved in …
There is this prevalent myth on tumblr eating disorder blogs that increased dopamine (DA) receptor activity or increased DA signalling causes anorexia nervosa. It has left me quite perplexed, as I have never come across a single paper that has shown increased DA activity causes anorexia nervosa. My research for this post also left me empty-handed. I have no idea where this myth comes from, but I thought I’d blog about what research on DA activity in anorexia has shown. This topic will take me a few (not necessarily successive) posts to cover. This first post is a very brief introduction to DA signalling.
First, what is dopamine?
DA is a neurotransmitter–a molecule that one neuron releases to another in order to send a signal. Dopamine is released from one cell (the presynaptic neuron) and binds to its receptors on the other (postsynaptic) neuron. There are five different DA receptors in the human brain, called D1, D2, D3, D4 and D5. (To add to the complexity, there is often more than one version of the receptor, called an “isoform.”) …
There have been some interesting discussions on the F.E.A.S.T. Facebook group over the past month regarding the role of genetics, personality traits, environmental factors and their role (or lack thereof) in the development of eating disorders and their prognosis. A parent group may seem like an unlikely forum for several hundred-odd comment threads on etiology; however, what we (caregivers, patients or clinicians) believe to underlie these disorders naturally informs our attitudes, decisions and choices with regards to treatment and our relationship to the disorders themselves:
Is this something they will have to manage their entire life?
Does anyone ever fully recover?
I had bulimia as a young adult and now my son has an eating disorder, too – did I pass on “bad genes”, bad habits, or is it a coincidence?
Is her rigidity and anxiety merely a side affect of starvation, or should we treat those as an underlying factor in her food refusal?
Is there any validity to the stereotyping of anorexics as uptight, overachieving perfectionists, and bulimics as impulsive, uninhibited hedonists?
There is at present …