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 feeling …
Hello Science of Eating Disorders readers! This is a guest post by Liz. Liz is a PhD Candidate in Psychology at the University of Toronto. You can read more about her research, interests, and eating disorder history on her “About” page.
And the usual “disclaimer”: Please keep in mind that I (Tetyana) give as much freedom as possible to guest writers and contributors to write about their own interests and viewpoints. That means that we don’t all necessary agree; there is no joint agenda. My primary reason for wanting more contributors is to widen the content, vary the writing styles, and negate the individual biases we all have. Our desire to understand, translate, and summarize peer-reviewed ED literature is what we all share in common.
Also, the Science of Eating Disorders blog is now one years old! My first post was published on April 3rd, 2012. Thank you everyone for reading, sharing, and commenting. Science blogging is a blast! I’ve learned a lot about eating disorders and science communication! Cheers! – Tetyana
The recent New York City …
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,
However, in the last two posts, I provided some evidence suggesting that dopamine systems are affected in anorexia nervosa. If one of the problems in anorexia nervosa is increased dopaminergic receptor activity or increased dopaminergic signalling, one way to augment that might be through the use of antipsychotics, which work, in part, by blocking dopamine receptors…
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 feeding behaviours, reward, motivation, …
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.”) The receptors …
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 no Grand Unified …
Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter that is involved in just about everything. It helps ensure proper cell growth, maturation and migration during development. Serotonin is also important in regulating emotions, cognitive functions, appetite, pain, circadian rhythms, and our endocrine system in adulthood. It is hardly a surprise then, that the serotonergic system seems to be important in bulimia nervosa (BN).
I’ve written previously about serotonin in restricting-type anorexia nervosa, so for this post I’m going to be shifting focus and talk about bulimia and binge-purge type anorexia nervosa (AN-BP).
The information in this post isn’t coming from a review paper. Instead, I’m going to be summarizing and explaining information from a chapter in a book titled Behavioural Neurobiology of Eating Disorders. In the chapter on serotonin and bulimia, Howard Steiger and colleagues propose a model for serotonin action in bulimia nervosa which takes into account “diverse hereditary and environmental influences… and helps account for heterogeneous traits seen in the bulimic population“.
Individuals whose eating disorders are characterized by the presence of binge-eating and purging display a …
Most people hate starving, hate prolonged hunger and suck at dieting. Anorexics, on the other hand, excel in these areas. How can someone like being hungry? How are they able to exert such “self-control” (as many non-ED people often say) over their food intake? Part of the answer might lie with serotonin. But don’t worry, there’s no “chemical imbalance” – it is much more complex than that.
In this post, I’m going to continue discussing the review article in Nature Neuroscience (2009) by Kaye et al., focusing on what is currently known or hypothesized about the role of serotonin in anorexia (reminder, findings Kaye et al focuses are specific to restricting-type AN and may not apply to AN-BP or BN).
BUT FIRST, A LITTLE NEUROSCIENCE
Serotonin (aka 5-hydroxytryptamine or 5-HT) is a neurotransmitter, meaning that it is a chemical messenger that cells in the brain use to communicate with one another. Neurons that make and release serotonin are located in a region called the raphe nucleus. These neurons project and “connect” to a variety of regions in the …