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 progesterone) becomes really important …
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 many …
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 Unified …
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 disorder have the other, …
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 people over an extended period of time, and …
Most people hate starving, hate prolonged hunger and suck at dieting. Anorexics, on the other hand, excel in these areas. How can someone like being hungry? How are they able to exert such “self-control” (as many non-ED people often say) over their food intake? Part of the answer might lie with serotonin. But don’t worry, there’s no “chemical imbalance” – it is much more complex than that.
In this post, I’m going to continue discussing the review article in Nature Neuroscience (2009) by Kaye et al., focusing on what is currently known or hypothesized about the role of serotonin in anorexia (reminder, findings Kaye et al focuses are specific to restricting-type AN and may not apply to AN-BP or BN).
BUT FIRST, A LITTLE NEUROSCIENCE
Serotonin (aka 5-hydroxytryptamine or 5-HT) is a neurotransmitter, meaning that it is a chemical messenger that cells in the brain use to communicate with one another. Neurons that make and release serotonin are located in a region called the raphe nucleus. These neurons project and “connect” to a variety of regions in the …
Hello all, Saren here. I’m honored that Tetyana asked me to be her co-contributor to ScienceofEDs, and am looking forward to collaborating on the project. My interests and background tend more towards the clinical; I don’t have the neuroscience training that she does, so I hope to bring a slightly different perspective while remaining committed to the research focus of the site. I can be reached at email@example.com with any questions, critiques or suggestions – I’d love to hear from you!
For my first post, I’m going to focus on one of the basic areas that much of the recent ED research aims to address:
We hear a lot about how eating disorders are complex syndromes with multiple causes. Articles in the popular press run the gamut from asserting genetic risk factors to proclaiming that Facebook causes eating disorders. In addition, disordered eating practices and poor body image are often conflated with the full-blown clinical disorders, further serving to muddy the waters.
Eating disorders have long thought to be caused by familial conflict and sociocultural pressures …