Why I No Longer Support Genetics Research into Eating Disorders – Part II (Illness and Recovery in a Neoliberal Society)

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 →

Why I No Longer Support Studying the Genetics of Eating Disorders – Part I

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

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Shared Genetics Between Disordered Eating and Periods (Menses)

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 … Continue reading →

Can Puberty Affect the Development of Eating Disorders?

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?… 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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Are All Anorexia Nervosa Patients Just Afraid of Being Fat? – Part 2

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 … Continue reading →

Does the Media Cause Eating Disorders? Disordered Eating in Iranian Women: From Tehran to Los Angeles

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:

  • does the media cause eating disorders
  • thin models on tv cause eating disorders to young girls
  • do models influence anorexia
  • ultra thin models causing eating disorders
  • magazine article eating disorders caused by the media
  • and the rare: media doesn’t cause eating disorders

I’m sure most of these search terms lead people to the … 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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Is Anorexia Nervosa a Version of Autism Spectrum Disorders?

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 … Continue reading →