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:
- Serotonin has a lot of functions in the body; it plays a role in regulating appetite (satiety), sleep, mood, behaviour, learning and memory, and a variety of other things
- Serotonin has been implicated in obsessionality, harm avoidance, and behavioural inhibition
- Alterations in serotonin function have been linked to many disorders, including depression, OCD, anxiety, and eating disorders
- Serotonin is made from tryptophan, an essential
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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
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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 … Continue reading →
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 … Continue reading →
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 … Continue reading →
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 … Continue reading →