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 stating that a particular fraction of an individual’s trait is caused by genetics.)
Adoption studies (scroll to bottom of link) provide a powerful alternative method to assess heritability and they …
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 topics supports an overall argument: focusing on singular explanations and solutions for anorexia, particularly through the vehement defense of any particular approach, obscures the complexity of the disorder, as well …
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 thin-ideal internalization?
One factor that’s curiously missing from the research is genetics. Can genetics play a role in explaining why some individuals are more prone to internalizing the thin-ideal …
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 as appetite, mood regulation, reward, anxiety, weight regulation, and so on. Then, they compare these genes in eating disorder patients and in healthy controls to try to identify any differences …
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, twin, and to a lesser extent, adoption studies.
In family studies, researchers are typically asking What is the probability that a relative of someone with an eating disorder …
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 associated with eating disorder symptomatology (Eastwood et al., 2002), though I don’t know if that finding has been replicated.
All of this is even more interesting because genetic effects on …
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 modulation?
Exploring this idea, Dr. Kelly Klump and colleagues sought to focus on the role of estradiol–the predominant estrogen during reproductive years in females. Estradiol (and other hormones, …
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 …
Refrigerator mothers or the idealization of thin models? Toxic families or toxins in our diets? Oh, if only determining the cause (because it has to be just one, right?) of eating disorders was that simple. All behaviour has a biological basis, a neurobiological correlate. The way our brains function—and the resulting behaviours — is due to complex interactions between our genome, epigenome, and the environment. Eating disorders do not have a single cause; we cannot put the blame solely on families, or thin models, vanity or genetics.
As a science grad student, I am interested in how non-scientists interpret scientific findings on mental disorders, particularly eating disorders. With respect to eating disorders, I am interested in how patients’ understanding of the science shapes the way they view themselves and their eating disorders, as well as how it shapes their treatment and recovery.
In a recent paper, Michele Easter wanted to find out just that; she wanted to know how patients with eating disorders view the increasing focus of genetics in eating disorders on ED stigma. She interviewed 50 women with a history …
[Note: This post has been translated into Croatian, link here
In 2009, Dr. Walter Kaye and colleagues published an article in the prestigious journal, Nature Neuroscience Reviews, titled “New insights into symptoms and neurocircuit function of anorexia nervosa”. [By anorexia nervosa, Kaye et al. limited themselves to restricting-type anorexics (AN-R), so some but not all findings may extend to bingeing-purging anorexics and bulimics] This review, which is lengthy and will take me a few posts to cover thoroughly, focuses on the “findings from pharmacological, behavioural and neuroimaging studies that contribute to the understanding of appetite regulation, reward, neurotransmitters and neurocircuits that are associated with AN.”
A striking feature of anorexia nervosa is the incredibly uniformity of traits and symptoms that patients experience, as well as the narrow range of onset. While the course of the illness varies from person to person, during the AN-R state, individuals exhibit very stereotypic presentation (and that, of course, may be due to malnutrition or common predisposing factors.)
Individuals with AN have an ego-syntonic resistance to eating and a powerful pursuit of weight