Your Body’s Response to Chewing & Spitting: The Role of Ghrelin and Obestatin

Shelly’s follow-up post on chewing and spitting, an often overlooked symptom in eating disorders. In her first post, Shelly discussed the prevalence of chewing and spitting among eating disorder patients. In this post, Shelly discusses some of the physiological effects of chewing and spitting. Enjoy! – Tetyana

Your body responds to food long before it reaches your stomach. The taste, smell, even the mere sight of food all act to trigger a physiological response, “priming” the gut by stimulating various enzymes required for proper digestion and absorption of nutrients. This is called the “cephalic response”, and it is mediated by a part of the nervous system that’s generally not under conscious control (the autonomic nervous system). Keep in mind, the actual consumption of food is NOT necessary to trigger this reflex.

As you may have already guessed, the act of chewing and spitting (CHSP) out … Continue reading →

Medical Complications of Purging in Bulimia Nervosa

Eating disorders are mental disorders with physical complications. Sometimes lots of them. I’ve blogged before about medical complications that are likely to come up in an emergency room setting, but that was a while ago. So I thought today I’d focus specifically on medical complications  that occur in bulimia nervosa (BN) as a result of purging (self-induced vomiting, laxative abuse, and diuretic abuse).

These complications are particularly important because patients with BN often appear healthy and can thus more easily hide their disorder, meaning that treatment is often initiated many years after disorder onset, and the duration of BN is often long, with recovery rates far lower than they should be (in one study, the 5-year recovery rate was a little more than 50%), which means that these complications can persist for many years.

I’ll go through some of the complications of self-induced vomiting, laxative abuse, diuretic abuse, … Continue reading →

Dopamine and Anorexia Nervosa: Tackling the Myths – Part IV (Treatment with Antipsychotics)

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.

Most importantly,

… the first line of treatment for underweight patients with AN should be

Continue reading →

Dopamine and Anorexia Nervosa: Tackling the Myths – Part II (Contradictory Findings in Preclinical Studies)

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 →

Dopamine and Anorexia Nervosa: Tackling the Myths – Part I (Intro)

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 … Continue reading →

Anorexia Nervosa: Can We Blame The Season Of Birth?

You might have heard that individuals born between the months of June – August (or sometimes March – August) have a higher chance of developing anorexia nervosa. But is it true? A lot of studies have been done to investigate the question of whether a season of birth (or a month) correlates with a higher risk of anorexia or bulimia nervosa. The results are inconsistent, weak, and fraught with methodological problems.

But first, how could seasons (or the average temperature during birth, or conception) have an effect on the etiology of eating disorders? What’s the hypothesis?

There seem to be two main ideas (summarized in Winje et al., 2012):

  1. alterations in neuropsychological function as a result of sunlight exposure during gestation or postpartum, maternal infections during pregnancy, or nutritional changes (seasonal variation in nutrients, vitamins)
  2. alterations in fertility/reproductive patterns of the parents due to cultural influences, disordered eating in the
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Chronicity in Eating Disorders: How Do We Define It and What Do We Do About It?

It comes as no surprise that the earlier eating disordered individuals receive treatment, the higher the likelihood that they will make a full recovery. In other words, the duration of the illness is inversely proportional with the likelihood of full recovery.

The problem is that a lot of eating disorders are not caught early. That a lot of people don’t have access to the treatment they need. Insurance will not cover it, their doctors don’t think it is a problem or won’t treat it, or there is simply no space. And even if there is space, and insurance will  cover it, dropout rates are incredibly high and treatment success is meager. The end result? Sometimes it is a success story – a full or partial recovery. But other times, the stories make headlines across the world, and not for good reason.

So then, what can we do about … Continue reading →

How Common Are Eating Disorders? Incidence, Prevalence and Mortality Rates

Six month of blogging and I have yet to do a proper post on the prevalence of eating disorders. I think it is about time. I see all sorts of numbers thrown around, often depending on the purpose of the article and the author’s bias. Is it 1 in 1000, 1 in 100, 1 in 20 or maybe even 1 in 2? Who is right?

Well, it is a tricky question to answer.

The number depends on how the particular study was conducted. Here are some factors that may influence the final rates: the population being studied, the sample size, the definition of eating disorder, the methods used by researchers to identify and screen for individuals with eating disorders, the number of years over which data is collected, and so on. In other words, a lot! That’s why in order to get a better sense of the true numbers, I … Continue reading →

Endophenotypes and Biomarkers in Eating Disorders: Genetic Underpinnings, Personality Traits, Vulnerabilities – Part 2

This post continues the discussion of the chapter on eating disorders by Carolina Lopez, Marion Roberts, and Janet Treasure from The Handbook of Neuropsychiatric Biomarkers, Endophenotypes and Genes (2009). Part 1 focused on neurotransmitter biomarkers, and this second part will focus on the neuropsychological biomarkers.

NEUROPSYCHOLOGICAL BIOMARKERS

Attentional biases

Attentional bias is the tendency for individuals to attend to or be distracted by emotionally relevant stimuli over neutral stimuli. Attentional biases have been observed in several studies:

  • Current AN and BN individuals showed bias towards food, body-related stimuli.
  • Past AN but not past BN showed bias towards body shape concerns.
  • Both current and “long-term recovered” AN showed “abnormally higher activation in the medial prefrontal and anterior cingulate cortices in response to food stimuli using fMRI [brain imaging]” (232)

These biases can be minimal but annoying: waiting in line at the pharmacy, staring into space and finding your focus … Continue reading →

Endophenotypes and Biomarkers in Eating Disorders: Genetic Underpinnings, Personality Traits, Vulnerabilities – Part 1

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
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