I spent the last weekend of October attending the Binge Eating Disorder Association Conference in San Francisco and it was awesome. I have attended several conferences over the past several years and each and every one fails to be inclusive. The discussion is always centred on the cisgender white straight middle to upper-middle class thin woman who suffers from anorexia. Every research presentation, every session, the same discussion just new material every conference.
Those involved in putting together BEDA this year decided to change the conversation and focus instead on diversity and including all the people that every other conference seems to leave out – and it was wonderful. Obviously I could not attend all of the sessions, so if you want more information check out the #BEDA2016 hashtag on Twitter.
It was clear from the opening session that this conference was going to be a completely different mood. This … Continue reading →
This is part II of posts on why I am highly skeptical of the argument that we need to understand the genetic basis of eating disorders in order to improve outcomes. If you would like to leave a comment, please read Part I as well.
I worry about the implications of focusing on genetics and neurobiology in identifying causes of and solutions to eating disorders in the context of a neoliberal society.
When I was an adolescent, finding out that eating disorders have a genetic component alleviated my guilt. Coming across Dr. Walter Kaye’s research into the neurobiology of eating disorders — the hypothesis that the drive to restrict may be linked to and reinforced by serotonin systems in the brain (here, here, and here) — provided me with a plausible biological explanation for why restricting made me feel calmer. It meant my eating disorder was … Continue reading →
I no longer support genetics research into eating disorders. Okay, that’s not quite right: I no longer support genetics research into eating disorders under the pretense that it will improve treatment outcomes or prevent eating disorders. I just don’t believe it. Moreover, I think emphasizing the need for a genetic understanding of eating disorders shifts focus away from research and, more importantly, from actions, that can yield much greater benefits much quicker.
It wasn’t always like this. In my third (junior) year of university, I wrote a mini-review on the genetic and neurobiological etiology (cause) of anorexia nervosa. In it, I argued that “in order to improve recovery outcomes, more specific treatments based on genetic and neurobiological evidence need to be developed.” I concluded by writing,
However, with the advent of large-scale genetic databases and worldwide collaboration among researchers resulting in larger sample sizes, the future of AN research
… Continue reading →
Genetics play an important role in the development of eating disorders and disordered eating behaviours. To date, many (over 30!) twin studies have been done and all but two found significant genetic effects on the development of eating disorders and disordered eating. However, no methodology is without limitations and tentative conclusions become more convincing when the findings are confirmed using different experimental approaches.
Twin studies, while they offer many advantages, are not that good when it comes to detecting shared environmental effects on a particular trait (literally, evens that happen to both twins and affect them in the same way). Fortunately, twin studies are just one of several different ways that researchers can use to study heritability. (A quick reminder: Heritability measures the amount of the variability in an observable trait/behaviour that can be attributed to genetic variation. This is NOT the same as … Continue reading →
I often hesitate to make broad, sweeping claims about the nature, cause, and experience of eating disorders and disordered eating. However, if there is one thing I feel absolutely certain saying about these disorders, it is that they are incredibly complex and multifaceted with no “one-size fits all” solution. So, I was quite excited when I came across a recent article by Michael Strober and Craig Johnson (2012) that explores the complexity of eating disorders and their treatment. Both authors have significant clinical experience treating eating disorders.
This article uses cases studies, literature, and the authors’ collective clinical experience to respond to some of the key controversies surrounding anorexia and its treatment. Among the major controversies that have come to light of late, they focus on two:
- Genetic/biological causation (Biologically-based mental illness – BBMI)
- Family-based treatment (FBT) as the best form of treatment for adolescents
The authors’ exploration of these … Continue reading →
The Tripartite Model of body image dissatisfaction postulates that three factors (peers, parents, and media) affect body image dissatisfaction and disordered eating through thin-ideal internalization and appearance comparison.
Thin-ideal internalization is the extent to which one accepts or “buys into” socioculturally defined beauty standards of thinness. The idea is that the more someone internalizes these standards, the more likely they are to engage in behaviours to achieve their “ideal”, and the more likely they are to develop an eating disorder.
A growing number of of studies have been done evaluating the validity of this model. Although I’m not well-read on the subject, it does seem like there is a growing number of studies showing an association between thin-ideal internalization and disordered eating practices.
But is the picture complete? Are peers, parents, and media the only or even the main factors that influence the extent of … Continue reading →
In my last post I talked about some methods that scientists use to study the genetics of eating disorders. I focused on a subfield of genetics called behavioural genetics (which you can think of as a field that attempts to understand, in part, the interplay of genetics and environment in behaviour). In this post I’ll shift gears and focus on molecular genetics. I’ll be working of the same review paper by Drs. Zerwas and Bulik (2011). Molecular geneticists study the structure and function of genes on a molecular level. For example, they try to understand how different mutations or alterations in the genetic code can affect protein function and lead to disease states.
GENETIC ASSOCIATION STUDIES
Genetic association studies are hypothesis driven. This means that researchers make a list of genes that are known to be involved in biological mechanisms or behaviours that are affected in eating disorders, such … Continue reading →
Today I thought I’d take the time to do an overview of what researchers know about the genetics of eating disorders and try to clear up some common misconceptions. The bulk of the content in this blog post comes from a very nice review paper published in 2011 by Drs. Stephanie Zerwas and Cynthia Bulik on the genetics and epigenetics of eating disorders. In an effort to keep blog posts short, this will be a multi-part mini-series.
When it comes to the genetics of eating disorders, there are two main questions that research ask: What is the relative contribution of genetic factors to eating disorder behaviours? And what are those genetic factors? I’ll talk about research attempting to answer the first question in this post and the second question in my next post.
In order to understand the role that genetics plays in influencing eating disorder behaviours, researchers use family, … Continue reading →
Puberty at an early age increases the risk for disordered eating behaviours such as bingeing and purging (Jacobi et al., 2004; Kaltiala-Heino et al., 2001). What’s more, the hormone estradiol moderates the risk of disordered eating behaviours. More precisely, in a group of twins with low estradiol levels, differences in disordered eating are likely due to environmental factors (such as family, school, friends), but in a group of twins with high estradiol levels, the differences in disordered eating are more likely due to genetic factors. (I blogged about it here.)
Essentially, estradiol partially moderates the extent to which genes affect disordered eating.
This is interesting because the estrogen system has a role in regulating body weight and food intake, influences eating behaviours during the menstrual cycle, and obviously plays an important role during puberty. Moreover, one study showed that estrogen receptor genes (proteins that bind estrogen) are … Continue reading →
Eating disorders typically begin in adolescence. One common explanation for this is that during adolescence females are increasingly exposed to the media, thin models, and dieting. While this is probably true to some extent, it doesn’t explain why the rates of eating disorders are quite low despite the high levels of exposure to thin models in the media. Out of 100 girls, only a handful develop eating disorders, yet all of them are exposed to the same magazines and TV shows.
This means there must be some other factors that differ between this group of girls. One hypothesis is that hormonal changes during puberty may modulate the genetic risk factors for eating disorders. These changes may “turn on” genes that predispose individuals to eating disorders. Previous research has shown that genetic factors modulate disordered eating (eating disorders have a high heritability), but how? What are the mechanisms of this … Continue reading →