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 disordered eating …
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, such as …
I bet you are thinking parents. Or media. Or thin models. Nope.
The SoB I am talking about is the season of birth bias (when the SoB pattern in a specific group differs from that of the general population.)
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?
I’m going to summarize some of the studies published on this topic, just to give you an idea of where the field is with regard to this question, and then I’ll briefly touch on some of the methodological problems in …
If you’ve been reading this blog for a while (or literature on this topic) you know the answer is no. I’ve blogged about this before, but I think it is a topic that needs a lot more coverage because the myths that all anorexia nervosa patients are just afraid of being fat, that they lose weight just to be thin, and that thin models are to blame for AN are still very common.
As you’ll see, I am not claiming that this isn’t true for some patients. Instead, what I am claiming is that it is not true for all patients.
And a big personal goal of mine with this blog is to broad the conversation about eating disorders. Let’s get away from stereotypes and painting all anorexia nervosa or bulimia nervosa patients in the same light. Let’s instead have meaningful discussions about research on eating disorders, about our experiences, and let’s develop a more comprehensive understanding of eating disorders that’s enriched by the research and the science, and our personal experiences as patients, friends, family members, partners, …
What is the impact of Western culture on eating disorders? Do images of thin cause eating disorders? I mean, it seems like such a nice and simple hypothesis. It makes intuitive sense: glamorize thin and make thin cool and BAM, everyone wants to be thin. It would be so much easier. Cause? Found. Solution? Easy: ban thin models. Unfortunately (or fortunately for me, since it gives me a lot to blog about) the answer is not that simple.
Just in the last couple of hours, some people who’ve ended up on the SEDs blog have searched:
I’m sure most of these search terms lead people to the blog post titled, Does Too Much Exposure to Thin Models Cause Eating Disorders? Anorexia, Bulimia in Blind Women? Since variants on this theme are common search queries, I thought I’d …
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.
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:
These biases can be minimal but annoying: waiting in line at the pharmacy, staring into space and finding your focus automatically pulled to the magazine headlines promising diet tips or drop a dress size in a week! even if those topics would not normally interest you. Or they might have a more intrusive …
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 …
Patients with anorexia nervosa often have difficulties recognizing and regulating emotions. This conclusion that is largely based on data from common tests such as Reading the Mind in the Eyes assessing emotion recognition, and questionnaires like Difficulties in Emotion Regulation Scale (DERS) assessing emotion regulation (see my post here). Although that study compared currently ill patients with healthy controls (thus raising the possibility that the resulting data was due to the effects of starvation or due to the chronic nature of the ED in the sample, ~7.5 year on average), there is some evidence that some of these difficulties persist post-recovery.
Individuals with autism (ASD, or autism spectrum disorders) also have difficulties with emotion recognition and regulation, leading some investigators to hypothesize that AN and ASD may share common etiology. Providing further support for this hypothesis are studies suggesting that AN might be overrepresented in ASD and vice versa. (That is to say, the prevalence of AN in ASD patients or vice versa is higher than the population mean.)
This doesn’t mean that all patients with one …
A really fun aspect of blogging is seeing what search terms lead people to my blog; a frustrating side-effect is not being able to interact with those people directly. This entry is, in part, an attempt to answer a common question that leads individuals to my blog. Common question or search queries are variants of the following (these are actual search terms that led to this blog, I corrected spelling mistakes): “do models cause eating disorders in women?”, “pictures of skinny models linked to eating disorders”, “do the images of models in magazines cause eating disorders?”, “eating disorders relating to thin models”, “psychiatrists thought on how skinny models are causing eating disorders”, “thin models are to blame for eating disorder.”
Well, you get the point.
I briefly started tackling the notions that the ”thin ideal” promoted by Western media is to blame for the prevalence of eating disorders and a related idea that all anorexics are afraid of becoming fat, in a previous post where I examined case studies of eating disorders in (mostly congenitally) blind women.
These assumptions, along with …
A not-so-recent, but interesting paper by Cynthia Bulik and colleagues outlines an interesting model for perinatal risk factors in the development of anorexia nervosa. The model ”focuses on adverse perinatal events and prematurity as risk factors for AN and encompasses the potential role of passive gene-environment correlation in perpetuating AN risk.”
Importantly, this model “provides intriguing data on a potential cycle of risk for at least a subset of individuals with AN.” The word subset is important: this model, if true – and we don’t know yet, undoubtedly applies only to a proportion of individuals that develop anorexia nervosa, so keep that in mind.
(In case you are wondering, because I was, perinatal period starts at 140 days of gestation and ends 28 days post birth, prenatal period is any time before birth.)
Trying to figure out the risk factors for anorexia, a rare disorder (<1% of the population), is challenging. One of the best ways to determine real risk factors (as opposed to early symptoms, such as dieting and overexercise) is to do longitudinal prospective studies: tracking lots of …