Consider this thought experiment:

Drop a person in a blender (since it's all hypothetical, go ahead and make it someone you don't like. Feel better? I bet you do!). Then, count all the total number of cells that are produced. Only one in ten of these cells will be human. The other 90%? Those are all microbes. If you look at the total number of genes in your human smoothie (NOT coming soon to a Jamba Juice near you), the numbers are even more skewed: only one in 100 genes are human. The rest are, again, bacterial. The total collection of all of these bacteria living in and on our bodies is known as the microbiome.

The idea isn't to gross out the card-carrying germophobes among us. But let's face it: we're just as much bacterial as we are human. Plenty of these microbes live on our skin, in our lungs and genital tracts. The mother lode of microbes, however, live in our gut. They are crucial to extracting energy from food, and these microbes are extremely sensitive to what we eat. Starving mice for just one day dramatically alters the composition of their gut microbes. Specifically, it decreases a type of bacteria known as Firmicutes. When researchers transplanted Firmicutes into the guts of lean mice, they rapidly gained weight (Crawford et al., 2009)

When it comes to eating disorders, there isn't much talk of microbes. There are the occasional papers from researchers like Sergei Fetissov about potential auto-immune responses in people with eating disorders, and some work on PANS (pediatric auto-immune neuropsychiatric syndrome) and anorexia, but generally, researchers haven't looked at the role of the microbiome in triggering or perpetuating an eating disorder.

Much work has been done in obesity research. Scientists have consistently found that people with a BMI >30 have different gut microbes than people with BMIs in the "normal" range. As well, bariatric surgery also significantly changes gut microbes as people lose weight, making them look more similar to the bacterial profiles seen in "normal weight" individuals. A more recent study in The ISME Journal proposed a microbiome diet: eating foods that would eliminate a type of bacteria called Enterobacter helped a person lose drastic amounts of weight in a short period of time (Fei & Zhao, 2012).

So how are microbes involved in eating disorders? No one really knows. Cindy Bulik has begun a study looking at this relationship, but the results still aren't in. Based on the studies above, it's reasonable to assume that ED behaviors (starving, binge eating, and/or purging) will have a significant effect on a person's microbiota. It still has to be measured, but I would bet a lot of money on it. The question is what do these microbial changes have to do with ED symptoms?

Imbalances in gut microbes in mice and rats have been found to alter patterns of risk-taking and anxious behaviors--something that also happens in people with EDs. They could also, perhaps, explain weight loss seen in anorexia and EDNOS. Maybe the initial restricting triggered a significant change in gut microbes that amplified the effects of malnutrition. Maybe they lacked a group of microbes that produced an important hormone regulating hunger and satiety. No one really knows.

One hint to the potential role of microbes in EDs comes from a study published today in the journal Science (Smith et al., 2013). The scientists studied the relationship between gut microbes and kwashiorkor, a form of severe malnutrition that occurs when a person doesn't eat enough protein. Of the 317 twin pairs from Malawi that the researchers followed for three years, half became significantly malnourished and 7% developed signs of kwashiorkor. Obviously, a lack of protein is crucial to the development of this disease but it's not the only factor as not everyone with a severely protein-deficient diet will develop kwashiorkor. Something else had to be going on.

First, the researchers treated twin pairs discordant for kwashiorkor (that is, one twin had it, whereas the other didn't) with "ready-to-use therapeutic food"- basically peanut butter on steroids. Twins with kwashiorkor had significantly different from nearby twins who (presumably) at pretty close to the same diet. The researchers found significant changes to the gut microbes in the ill children with the use therapeutic food. Discontinuing the therapeutic food caused a regression in the functioning of the gut microbes.

The kicker is this: when the researchers fed mice a standard Malawian diet and inoculated them with microbes from the guts of malnourished children, they rapidly lost weight and also developed kwashiorkor. This happened despite the fact that their diets contained adequate calories. One of the reasons that the researchers believed the therapeutic food is so effective at treating kwashiorkor is that it helped restore normal gut microbes.

To say what effect restoring normal gut flora will have on ED symptoms remains to be seen. Probiotics are a hot item, but much of the research is fairly overblown. There's definitely still potential there, and we need to know more about which populations of people are likely to benefit and which aren't. But it's an interesting idea, and I think we need to know a lot more about the role of the microbiome in the development and perpetuation of EDs.

In closing, a quote from scientist John Rawls in an interview with Scientific American:

“We are in the midst of a revolution of our ability to describe the composition and physiological potential of these bacterial communities...What we can begin to speculate on, though, are the different types of relationships that might be taking place. We know gut microbiota enhance our ability to extract calories from complex carbohydrates, which is clearly a mutually beneficial relationship. But it’s thought that all vertebrates have the capacity to digest and absorb other types of nutrients, such as lipids, proteins and simple carbohydrates, so it’s not readily clear how we could enter into a mutually beneficial relationship with bacteria with regard to those nutrients."

Lest you think I'm normal, let me provide you with yet another example proving otherwise. When my print version of the International Journal of Eating Disorders arrives in the mail, I totally geek out. Last month was no different. I've generally seen most of the articles before, as they are published online before they appear in the print journal, but I like sitting down on my couch with the journal and reading what's new.

What struck me about one particular study in last month's journal was not the study itself, but rather a reaction to it on Facebook.

What the study found

The researchers, which included recovering ER physician Suzanne Dooley-Hash, evaluated a series of 942 adolescents (ages 14-20) who showed up in the emergency room for any reason. They were given a computerized questionnaire, which evaluated (among other things) them for the presence of an eating disorder. The SCOFF questionnaire is below. Marking yes to 2 or more questions was considered positive for an eating disorder.

The researchers also assessed the patients' BMIs, and the presence of tobacco, alcohol, and substance abuse. Interestingly, BMI was associated with the presence of an eating disorder, but maybe not in the way you would expect. The teens with a BMI over 30 were actually most likely to test positive for an eating disorder- they were 3.2 times more likely to show signs of an ED than so-called "normal weight" adolescents.

Overall, the researchers found that 16% of the teens shows signs of an ED, and that nearly 30% of those with ED symptoms were male. Frankly, I think those numbers are a little high, as the SCOFF seems to evaluate a lot for disordered eating as much as a clinical eating disorder but that's outside the scope of this blog post.

But what's the denominator?

This, of course, brings me to the Facebook comment. In full, it read:

In the "International Journal of Eating Disorders" that came in the mail today I read a fascinating study on the prevelance and correlates of eating disorders among emergency department patients ages 14-20.  

They found that in a screening of nearly 1,400 patients that 16% screened positive for an eating disorder. That is much higher than the average of .5-1% for AN, 1-3% for BN, and 3-5% for EDNOS typically reported. In addition they found nearly 27% of those screened were male, much higher than the less than 10% typically reported. 

This supports much of the research we see that ED is on the rise, and that boys and men are just as much at risk.

Sad. We have much work to do.

 Here's the thing: the researchers were screening adolescents who were in the emergency room. This does not mean that that 16% of teens have eating disorders. It means that 16% of patients who were in this particular emergency room answered yes to at least two out of five questions on a survey.

Let me repeat: this study does NOT mean that 16% of teens have an eating disorder. Although the author of this comment didn't directly say this, it was sort of implied in the part where they said that "EDs are on the rise." One would likely expect that teens in the ER would be more likely to have an ED given the high levels of physical and psychiatric co-morbidity that they have. My guess is that people with EDs are much more likely to wind up in the ER than people without EDs. As well, teens are at higher risk for EDs and disordered eating, which further explains the high numbers.

Nor is this evidence that EDs are on the rise. I don't think there have been previous studies looking at the percentage of adolescents presenting to an ER who have ED signs and symptoms, so it's impossible to say whether these numbers are more or less than before. As well, the current research on the number of EDs in the US or elsewhere isn't all that great, so I'm rather cautious about saying whether EDs are on the rise. My bet is that we are certainly more aware of them, and so people might be more inclined to seek care (or be pushed into care, as the matter might be), but again, that doesn't mean that EDs are more common.

When evaluating these statistics, it's important to remember the denominator; that is, the portion of the population that the researchers are surveying. Here, it was adolescents in the ER. I bet you could find 100% prevalence on an inpatient eating disorders unit. We rightly should not be alarmed that so many people have eating disorders if these statistics were surveyed. Well, obviously people being treated for eating disorders almost certainly have an eating disorder.

The study is important in that it shows that ER docs can play an important role in identifying EDs. Most of them have their heads too far up their asses to actually do anything about it, but it is good and useful information. I don't like the SCOFF survey (like, at all), but it is quick and dirty, so I understand why they might have used it. Other than that, I think the study is very useful, but we all need to be careful how we interpret and talk about these results.

I don't know if you've seen the headlines (the story has been making the rounds in the psychology circles for the past day or two), but a study just came out that looked at the relationship between body dysmorphic disorder and nose jobs. The study found that one-third of people who wanted a nose job for cosmetic reasons had moderate to severe symptoms of BDD. Of those who wanted a nose job for medical reasons (to improve breathing, etc), 2% had been diagnosed with BDD.

Except that's not how the study was reported. Instead, headlines like "Nose job patients often mentally ill, study says." An excerpt from this piece below:

Of patients who were seeking the procedure to correct a breathing problem, only about 2 percent showed symptoms of BDD. But of those who wanted a nose job for cosmetic reasons, 43 percent showed symtoms of the disorder.


BDD was especially common among people with a history of mental illness, as well as those who had already had a nose job and were seeking “revision” surgery.

The problem, as John Grohol pointed out on the World of Psychology blog, is that "symptoms of BDD" aren't the same as being diagnosed with BDD. It's a subtle difference in words, yes. But it's a major difference in what we're actually talking about.

I had symptoms of the flu several winters ago. High fever, muscle aches, chills, feeling utterly crap, all with a sudden onset. Classic flu symptoms. Except a flu test revealed that whatever I had wasn't the flu. It looked a lot like the flu, it had the same symptoms as the flu, but it wasn't caused by the influenza virus.

Someone can have symptoms of depression (low mood, feeling hopeless), but not actually have clinical depression. Same with BDD. Same with EDs, too. The scales and questionnaires used in research aren't diagnostic tools. They can give you an idea whether you should see an actual living, breathing professional for evaluation and a potential diagnosis, but they don't say whether you actually have the condition.

It's not the public's job to know this. I'm not saying scientists shouldn't use these measures simply because they are so frequently misinterpreted by laypeople and journalists alike. But I am saying that journalists and editors need to know the difference. It's responsible reporting.

It happens with eating disorder stories all the time. Most commonly, it happens when people conflate disordered eating with eating disorders, or the scores on a survey with an actual diagnosis. The problem is that most people don't know there's a difference between these two things, or that the difference really matters.

Of course we would expect that people seeking nose jobs have higher concern and focus on their appearance. They are, after all, dropping thousands of dollars in an attempt to, you know, look better. But focus on your appearance isn't the same as BDD, and it's offensive to those who are suffering to make the two things equivocal. It's like saying someone who is obsessed with their weight has an eating disorder. They're not the same. At all.

We need to start distinguishing between these two things so that we stop trivializing deadly mental illnesses as little more than cultural fads.

I received a message from the University of Chicago ED Treatment Program that let me know of the following treatment opportunities:

We provide free treatment services through our NIH-sponsored research studies. We are currently recruiting for the following studies:


Adolescent Bulimia Nervosa Treatment Study: This study provides no-cost outpatient treatment to adolescents suffering from bulimia nervosa. To be eligible, participants must be between the ages of 12-18, have a diagnosis of bulimia nervosa or partial bulimia nervosa, live with at least one parent/guardian, and be prepared to participate in up to 6 months of no-cost treatment along with assessments. Participants can receive up to $200 if all assessments are completed. For more information, please contact Colleen Stiles-Shields at 773-834-5677 or bulimia@yoda.bsd.uchicago.edu.

Adolescent Overweight Treatment Study: This study provides no-cost outpatient treatment for adolescent obesity. To be eligible, participants must be aged 13-17, must be overweight, living with at least one parent/guardian, and be willing to participate in up to 24 weeks of no-cost treatment for weight loss as well as complete assessments. For more information, please contact Kali Ludwig at 773-834-0360 or kludwig@bsd.uchicago.edu.

Adult Anorexia Nervosa Treatment Study: The University of Chicago is conducting a National Health funded research study designed to develop and refine a family-based treatment manual for young adults (aged 18-30 years) with Anorexia Nervosa as well as assess the feasibility of this out-patient psychotherapy. Treatment involves up to 6 months of cost-free individual and family therapy sessions. Interested individuals may contact our Research Coordinator at (773) 834-9120.

If you would like to find out more information about our general outpatient eating disorders clinic or educational services that our team may be able to provide, please contact our clinic coordinator, Leah Boepple, at 773-702-0789.

You can also visit our website at www.eatingdisorders.uchicago.edu or our Facebook page at http://www.facebook.com/#!/pages/University-of-Chicago-Eating-and-Weight-Disorder-Program/112762265461075.

Carrie's note: As always, participating in a research study has risks and benefits.  Click here to get more information on participating in clinical trials.

I don't know whether this means I'm definitely in the right career, or just a glutton for punishment.

I started another blog.  A science writing blog.

"Somewhere, something incredible is waiting to be known." --Carl Sagan

I know that the only way to get better at writing is to actually do it.  And there are so many cool things to write about, things that I won't get the chance to cover for, you know, money.  That's where this blog comes in.  It's my chance to write about all of the cool things that I normally wouldn't write about.

I probably won't be blogging all that much at first.  I'm trying to pack and move, and deadlines for paying work will always take prescedence.  So, too, will ED Bites.  It's my baby.  It's not going anywhere.  I've put way too much effort into this blog to let it wither away.

But I also need to start putting more effort and time and energy into non-ED things.  I don't think this blog is holding me back--far from it.  Yet I also don't want to be known just for my ED work.  It doesn't bother me that most of the world knows me for ED-related and recovery things.  At the same time, that's not all I want the world to know me for.  It's been a big part of my life, but I hope to make it a much smaller part of my life.

Hence this blog. 

It's a recovery step, in a way, even though it really has nothing much to do with the eating disorder at all.

My latest story for Scientific American, More Than Meets the Mirror, is actually relevant to this blog (it doesn't happen very much!).  It's about the relationship between body image and what's known as interoceptive awareness.

Are you cold?  Thirsty?  Hungry?  Short of breath?  Whatever your answer, you used interoceptive awareness to answer the question.  Previous research has linked interoceptive awareness to the insula, and people with eating disorders have been shown to have deficits in both of these areas.  But that didn't mean the two were necessarily related.  After all, I have red hair and green eyes, but my green eyes didn't cause my red hair (for that, I thank Garnier Nutrisse Honeydip).

So a neuroscientist at the University of London devised an experiment where he tested students' interoceptive awareness by having them measure their heartbeat without taking their pulse.  Then he used a trick known as the rubber hand illusion to trick the students into thinking that a rubber hand was actually a part of their body.  Those students with low interoceptive awareness were more susceptible to the rubber hand illusion.

From the story (I do feel a little weird quoting myself, but whatever):

"People with low interoceptive awareness might have a less strict distinction between what is 'my body' and what is the external world," Tsakiris says. "They might be ruled more by vision, rather than by internal sensation." Previous studies have also found that people with anorexia have an impaired ability to sense internal cues, making the results of this new work useful for understanding and potentially treating severe body-image disturbance.

To be sure, the study used a small sample size and has not yet proved causation, but "if we can train people to sense their interoceptive states," Tsakiris says, "it might make a change in their body image. An interesting avenue for future research would be to see if improving interoceptive awareness impacts different areas of these disorders."

This study just irritated me: Psychiatric 'diseases' versus behavioral disorders and degree of genetic influence

The study's premise was that

"Psychiatric conditions in which symptoms arise involuntarily ('diseases') might be assumed to be more heritable than those in which choices are essential (behavioral disorders). We sought to determine whether psychiatric 'diseases' (Alzheimer's disease, schizophrenia, and mood and anxiety disorders) are more heritable than behavioral disorders (substance use disorders and anorexia nervosa)."

...And what do they think drives behaviors? Have these researchers even thought about what anorexia actually is? No, it's not a bunch of skinny dieting champs. It's about being scared to eat. Which strikes me as less of a behavior and more of something arising "involuntarily."

I've heard some people say that they chose to be anorexic, but I would say that for the vast majority of people, they didn't choose their eating disorder. I know I didn't. Did I make the choice to lose a few pounds and exercise more? Yes, I'm not denying it. But choosing to head to the gym regularly is totally different than choosing to be anorexic. The first I will concede; the second I most definitely will not.

It frustrates me. It really does, especially because this is a scientific study carried out by actual professionals. I can grit my teeth and try and explain to Jim Bob that I wasn't randomly deciding to live on Diet Coke and look like a model because he very well might not know better. But psychiatric specialists? Seriously?

Interestingly, they didn't consider OCD in their spectrum of diseases, which would be interesting since it involves what they would term "involuntary" symptoms (obsessions) as well as chosen behaviors (compulsions). Nor did they address how people with depression are often told to cheer up and snap out of it, which implies that it really is a choice.

There are endless choices I've had to make as I've recovered from my eating disorder, although many of them were a choice amongst lack of alternatives. I've been told recovery is a choice, and although I don't think that's wrong, I don't think it's that simple. It's not as if recovery is one single choice, and it's not as if our brains always have the same capacity to make these choices as we move through recovery. There is some small amount of choice when my brain is compelling me to engage in ED behaviors or OCD behaviors, and I can see that now that I'm no longer in it on a minute to minute basis. But in the moment? I didn't see a choice, and my brain chemistry tipped the scales so heavily in favor of the disordered behaviors that I couldn't un-choose my disorder without a serious amount of support.

Ultimately, the study didn't find that "behavioral disorders" were any less heritable that psychiatric "diseases." They found a 60% heritability rate for anorexia, although other studies have found rates of 70% and Walt Kaye frequently uses an interval of 60-84% heritability (I believe this can be found in his Maudsley Parents lecture here).

The authors concluded:

No systematic relationship exists between the disease-like character of a psychiatric disorder and its heritability; many behavioral disorders seem to be more heritable than conditions commonly construed as diseases. These results suggest an error in 'common-sense' assumptions about the etiology of psychiatric disorders. That is, among psychiatric disorders, there is no close relationship between the strength of genetic influences and the etiologic importance of volitional processes.

Maybe that's because these "behavioral disorders" really are diseases...

In attending many presentations and talks about eating disorders, one of the more fascinating topics I've heard mentioned was interoceptive awareness. Interoceptive awareness (IA), as a research article on the subject succinctly put it in the title, is "the sense of the physiological condition of the body." What this means is that when you sense things like "pain, temperature, itch, sensual touch, muscular and visceral sensations, vasomotor activity, hunger, thirst, and 'air hunger,'" you are using IA. The input is internal, unlike other senses that are more external. Visual input comes from outside your body; a sense of exhaustion is more internal. Furthermore, an ability to recognize your emotions is also considered part of IA, and all of these IA tasks occur in an area of the brain known as the insula. Wikipedia tells us that the functions of the insula "include perception, motor control, self-awareness, cognitive functioning, and interpersonal experience."

Scientists have long speculated that people with eating disorders have impaired IA. A recent research review article by Walter Kaye examines the evidence of dysfunction in both the insula and in IA as one of the drivers of ED behaviors (Kaye, Fudge, and Paulus, 2009). Research on the relationship between EDs and IA dates back to this paper from 1978 by Garfinkel et al. Impaired IA would help explain how a person with AN might be able to continue to starve themselves--their hunger cues might be impaired. Or how someone with BN might be able to continue to binge--their satiety cues might be impaired. Furthermore, people with eating disorders often struggle with identifying emotions, body size and shape, and fulfilling other biological needs (such as sleep). Poorer IA is also associated with poorer ED outcome (Lilienfeld et al, 2006). I've blogged on my own (mis)adventures with IA here.

I'm still not very talented at figuring out whether I'm hungry or full, whether I'm tired and need a nap or just need to stretch my legs. Some of the hunger/satiety issues were probably thrown off by the eating disorder, but some of it may just be the way I'm wired. I've been in the midst of several full-blown hypoglycemic episodes (feeling faint, shaking, sweating, vomiting) and thinking "How could that be? I don't feel hungry." Obviously. I wasn't trying to delude myself- I've had ED-induced hypoglycemic episodes where I knew damn well it was because I hadn't eaten and I played the green-eyed ingenue. But there were plenty of times where I delayed a meal because I didn't feel hungry and then WHAM! Which is a great example of impaired IA, if nothing else.

A new study published this week found that levels of Brain Derived Neurotropic Factor (BDNF; which encourages the growth of new neurons and helps existing ones thrive) were correlated with interoceptive awareness and maturity fears in people with anorexia and/or bulimia (Mercader et al, 2010). Specifically, the researchers found that higher levels of BDNF were correlated with lower interoceptive awareness and higher maturity fears. The authors suggest that BDNF levels may play a role in regulating ED psychopathology via impaired IA.

Previous research has explored a link between BDNF and both anorexia nervosa and bulimia nervosa.

I'm not thinking that testing BDNF levels are going to become standard of care anytime soon--BDNF is associated with impaired IA but that doesn't tell us much. Does BDNF have an affect on IA or is it just a bystander? How might BDNF affect IA? Does decreasing BDNF levels increase IA?

Like so much research, this paper raises more questions than it really answers. Still, I find it all very interesting.

Our data suggest that BDNF levels may influence the severity of the ED by modulating the associated psychopathology, in particular through the impairment of interoceptive awareness.

This recent study, titled "Psychopathology in underweight and weight-recovered females with anorexia nervosa," beautifully articulates something that I've struggled to put into words. The study found that weight recovery in people with AN dramatically decreased psychopathology.

No, no--it's not that weight restoration cures everything! Because my life right now is an obvious example that this isn't exactly true. I would never say that weight gain isn't necessary, just that it's the necessary first step towards a meaningful recovery. If weight gain "cured" anorexia, then there wouldn't be the tremendously high rates of relapse that we see. The difficulty with weight gain is consequently keeping the weight on for long enough to get physically used to your new body and to begin the mental healing process.

But I digress.

The reason I find this article so incredibly interesting is how it managed to examine the relationship between somatic factors (ie, weight) and psychological factors (ie, ED psychopathology). Usually, the mind/body connection is seen as something very heebie-jeebie and New Age-ish, an idea sprung from the mind of a few pot-smoking hippies reeking of patchouli. But the brain was connected to the rest of the body- at least the last time I checked. The brain is an organ, just like your heart or your liver.

The mind/body separation in Western culture has been around for hundreds of years and has resulted in some rather interesting separations in medicine. The need for mental health parity is one of them, although that could also be interpreted the machinations of a bunch of cheap-ass insurance companies. With eating disorders, the assumption was that the ED thinking caused the behaviors that caused malnutrition and weight loss. It was a one way street. Although this is somewhat true (most people with AN don't start out malnourished no matter how catastrophically they end up that way), the opposite is also true. Low weight can cause ED thinking, which causes ED behaviors and a further increase in malnutrition, and I think that's what they call The Perfect Storm.

The body and mind aren't separate. Your brain uses approximately one quarter of the calories you eat (500/day) and is essentially a glucose hog. If you starve your body, you starve your brain. I managed to shrug many of the physical effects of anorexia off, but the cognitive effects really got to me. The knowledge that I can't preferentially shunt calories to my brain has helped me resist urges to restrict. I know I'm not the next Einstein, but my job requires a lot of intense, deep thinking, and anorexia would grind that to a halt. I don't miss being caught in the circular ED thinking, worry about what I ate, what I will eat, what I might eat, and exercise and fat grams and everything. If I delay my meals or snacks for any length of time, I notice a return of the anxiety and ED thinking, even if I don't notice a difference in my hunger levels.

It seems odd to think that something as simple (though fraught with challenges for those of us with ED) as eating could improve state of mind. It's not a cure, but it should stop being so surprising to so many people.

(An interesting note: the one area of psychopathology that didn't improve with weight gain was perfectionism, which emphasizes how this is a long-standing personality feature of many with EDs rather than limited to the time when one is acutely ill with ED.)

Although the research isn't that new, there was a wonderful write-up on Walt Kaye's brain imaging research in the Psychiatric Times (creatively titled Anorexia and Brain Imaging).

A short excerpt:

...insights into the ventral (limbic) and dorsal (cognitive) neural circuit dysfunction, perhaps related to altered serotonin and dopamine (DA) metabolism, may help explain why individuals with anorexia often report that dieting reduces their anxiety while eating increases it and why they worry about long-term consequences but seem impervious to immediate gratification and unable to live in the moment.

Many women diet in this culture, but relatively few (0.5%) have anorexia, Kaye told Psychiatric Times. “Why is that? Well, you pretty much have to have a certain temperament and personality in childhood to be vulnerable for . . . an eating disorder,” said Kaye. “Not everyone who develops anorexia has all these traits in childhood, but most have one or more of them,” he said. “These traits include harm avoidance, anxiety, behavioral inhibition, difficulty with set shifting [easily moving from one mental set to another], a tendency to focus on details rather than the big picture, and perfectionism.” Even after recovery, these personality and temperament traits persist, pointing to underlying neurobiological factors.

...Kaye said that evidence from imaging studies suggests that disturbances in the serotonergic system might contribute to vulnerability for restricted eating and behavioral inhibition as well as a bias toward anxiety, particularly excessive concern with consequences. Meanwhile, DA dysfunction, particularly in striatal circuits, may contribute to altered reward, decision making, stereotypic motor movements, and decreased food ingestion.

The article isn't simple--the magazine is aimed at psychiatrists, not otherwise clueless neuroscience geeks like yours truly--but it's written very clearly, and Google helped me figure out what terms I didn't know. If you ever want a good handout on up-to-date information on anorexia for medical professionals, this would be a good one to print and keep on hand.

New research on people with body dysmorphic disorder shows that their brains focus on the details of their faces, rather than taking in the face as a whole. The study, titled "Abnormalities of Visual Processing and Frontostriatal Systems in Body Dysmorphic Disorder," was published in the most recent issue of Archives of General Psychiatry.* CNN covered the story, an excerpt of which is below:

It turns out that people with this condition have abnormal brain function when it comes to looking at pictures of their own faces, according to a new study led by Feusner and published in the Archives of General Psychiatry.

When viewing themselves in photographs, patients with BDD underutilize parts of the brain used in seeing the face's overall shape and size, he said.

"If you just see the pieces of your face, and not seeing how they fit into the whole, then it's going to look distorted," he said. "That's how we interpret the findings."

What is especially interesting are the similarities between BDD and anorexia. Similar to what this study found in people with BDD, previous research has found that people with anorexia tend to focus on the details, which leads to a trait known as Weak Central Coherence (Southgate, Tchanturia, and Treasure, 2008). People with AN also show abnormalities in neural functioning when looking at images of themselves, but not other people (Sachdev et al, 2008).

More from the CNN story:

"...the part of the brain that helps guide behavior and maintain emotional flexibility, the frontostriatal systems, had unusual activation patterns.

"What we think may be happening is that they may be seeing details, perhaps even seeing details normally, but that they're not able to contextualize it," [Fuesner] said...The study is "groundbreaking" in its demonstration that patients with BDD are too focused on the details aren't able to see the whole picture when they see themselves, said Sabine Wilhelm, director of the BDD Clinic and Research Unit at Massachusetts General Hospital, who was not involved in the study. This can be observed anecdotally in treatment, but this study confirms it at the level of brain processing, she said.

Feusner's previous research found that when BDD patients viewed the faces of other people -- not their own faces -- the brain's left hemisphere, associated with categorization and details, was more more active. Healthy individuals used the right hemisphere, the part of brain that processes more holistically.

It is too early to directly apply the findings to treatment, but one possibility is that patients with BDD could be retrained to see their own faces, he said.

Considering that people with BDD show many of the same difficulties in executive functioning (i.e., "a loosely defined collection of brain processes which are responsible for planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions, and selecting relevant sensory information.") as people with AN, perhaps the underlying neurological similarities shouldn't be surprising.

The Semel Institute at UCLA is currently recruiting subjects for a study to compare neural processing in people with BDD, people with AN, and healthy controls. Click here for more information- I will phone the study site tomorrow as I am interested in participating and I will post more information as I get it.

*I haven't yet been able to get ahold of the full-text of this study- my alumni association dues need to be updated before I can get a copy, so I apologize.

Two studies were published this week that made the connection between genetic variations and anxiety disorders in both humans and animals.

One study, published in the journal Science, found that mice and humans with the same mutation in an anxiety-related gene behave similarly. The study, titled "A Genetic Variant BDNF Polymorphism Alters Extinction Learning in Both Mouse and Human," sounds almost deliberately obtuse, but the results are interesting. Lab rats (or in this case, lab mice) are often used in research for any number of reasons, which include the fact that they are small and relatively easy to handle, they reproduce quickly, and over a century of intense breeding and research has enabled researchers to know an animal's exact genetic profile. Many studies in behavioral neuroscience use mice and rats for these reasons, and also because it's generally difficult to get humans to participate in many of these experiments (which are often ended by autopsy so the brain can be examined). From a genetic standpoint, there aren't a whole lot of differences between a human and a mouse. Many of the tasks we both have to complete--digesting food, eliminating waste, maintaining homeostasis--are pretty darn similar, so researchers have hypothesized that the neural circuits controlling behavior in mice and people are actually similar.

This most recent study looked at a variation in the gene that makes Brain Derived Neurotropic Factor (BDNF), a protein responsible for brain growth and development. The interesting result was that the mice and humans who had this variation had similar behaviors. From a Science Daily press release:

To make their comparison, the researchers paired a harmless stimulus with an aversive one, which elicits an anxious-like response, known as conditioned fear. Following fear learning, exposure to numerous presentations of the harmless stimulus alone, in the absence of the aversive stimulus, normally leads to subjects extinguishing this fear response. That is, a subject should eventually stop having an anxious response towards the harmless stimulus.

"But both the mice and humans found to have the alternation in the BDNF gene took significantly longer to 'get over' the innocuous stimuli and stop having a conditioned fear response," explains Dr. Fatima Soliman...

...[Researchers] found that a circuit in the brain involving the frontal cortex and amygdala -- responsible for learning about cues that signal safety and danger -- was altered in people with the abnormality, when compared with control participants who did not have the abnormality.

"Testing for this gene may one day help doctors make more informed decisions for treatment of anxiety disorders," explains Dr. Francis S. Lee.

Specifically, it may help therapists tailor approaches to treating anxiety such as exposure therapy, which is an empirically supported treatment for a variety of anxiety disorders, such as phobias and PTSD.

"Exposure therapy may still work for patients with this gene abnormality, but a positive test for the BDNF genetic variant may let doctors know that exposure therapy may take longer, and that the use of newer drugs may be necessary to accelerate extinction learning," explains Dr. Soliman.

BDNF has also been associated with both anorexia nervosa and bulimia nervosa.

In a completely separate study, researchers have identified a genetic mutation that results in compulsive behaviors in a wide variety of animals. From a New York Times article on the study:

Researchers studied Doberman pinschers that curled up into balls, sucking their flanks for hours at a time, and found that the afflicted dogs shared a gene...the findings [have] broad implications for compulsive disorders in people and animals.

Dr. Dodman and his collaborators searched for a genetic source for this behavior by scanning and comparing the genomes of 94 Doberman pinschers that sucked their flanks, sucked on blankets or engaged in both behaviors with those of 73 Dobermans that did neither. They also studied the pedigrees of all the dogs for complex patterns of inheritance. The researchers identified a spot on canine chromosome 7 that contains the gene CDH2 (Cadherin 2), which showed variation in the genetic code when the sucking and nonsucking dogs were compared.

The statistical association led to further investigation to determine for which protein the gene contained instructions. It did for one of the proteins called cadherins, which are found throughout the animal kingdom and are apparently involved in cell alignment, adhesion and signaling.

Cadherins have also been recently associated with autism spectrum disorder, which includes repetitive and compulsive behaviors...

...“Stress and anxiety, as well as physical trauma and illness, can trigger repetitive behavior that then takes on a life of its own,” Dr. Ginns said.

But he believes that in many cases there is an underlying genetic predisposition that responds to environmental stimuli in such a way that once-normal behavior turns into something pathological. Those genetic dispositions may differ markedly between different behaviors.

Considering the links recently postulated between anorexia and autism as well as anorexia and OCD, these results may one day have an effect on our understanding of eating disorders.

I thought about including this piece of research in last week's smorgasbord, but I thought it was so important that I wanted to make sure it got its solo time in the limelight.

Determining target weights in people with eating disorders has never been easy. Many doctors lowball the weight so they don't scare off the patient. Which is nice (remember the phrase about the road to hell being paved with good intentions?) but it also really twists the sufferers mind and leaves them only 90% well. No one would settle for removing 90% of a tumor just to make a cancer patient feel better in the moment, so why people are very willing to tolerate sub-optimal target weights is beyond me.

This has been an issue with me because I'm fairly muscular, and I weigh more than I look like I do (a friend described me as small but solid). So the old formulaic 100-pounds-for-five-feet-and-five-pounds-for-every-inch-over left me at a weight where I had already lost my period on the way down. I was more than happy to stay at the inappropriately low weight, not the least because I got to skip out on the monthly tampon shopping sprees. It also left me deeply entrenched in the eating disorder.

There are also other treatment providers who would provide an accurate target weight if only they knew what it was. In younger children, in those who have been sick longer, and in those who don't have growth charts, even the best physician can be flummoxed. The organization FEAST has some good information on setting target weights, as does the Kartini Clinic, and although these methods are informed by science, they are still as much of an art as anything.

But we might have a new tool to help with this. A recent study from the European Eating Disorders Review found more objective ways to help determine target weight in a study titled "Predicting the weight gain required for recovery from anorexia nervosa with pelvic ultrasonography: An evidence-based approach."

The abstract of the study summarizes the outcome of the study rather well:

Transabdominal pelvic ultrasound scanning (U/S) offers a more objective method of ascertaining physical well being by the ability to determine reproductive maturity. This study aimed to explore the correlations between the maturity grading on pelvic U/S and weight for height (WfH) ratios and body mass index (BMI) percentiles. Ultrasound studies were performed in 72 female adolescents (aged 11-17 years at intake) with AN. Scans were graded for maturity using published parameters of pelvic maturity and compared with the patient's WfH ratio and BMI percentile. In our sample was a wide variation of WfH ratios and BMI percentiles at each grade of maturity. This supports the view that arbitrary targets for weight, WfH ratio or BMI percentile are likely to be unnecessarily high for some patients and too low for others. We recommend that targets be based upon baseline pelvic U/S grading and follow-up scanning.

This study will probably need to be replicated before it can become commonplace, but I am so glad that there are now evidence-based approaches for helping to determine target weight that are more effective than a coin toss or one-size-fits-all approach.

At an initial glance, a new study from the Journal of Consumer Research appears to have absolutely nothing to do with eating disorders. It wasn't about magazines or models or the purchase of diet products. The title of the paper had the rather bland-sounding titled of "Counteractive Construal in Consumer Goal Pursuit." That sounds as exciting as organizing my sock drawer. Rather, what caught my eye was the title of a news brief about the research titled "Resisting temptation is easier for those who exaggerate the threat."

And I thought, "Huh. That sounds a lot like what happens in eating disorders."

It sure does.

The authors of the research did four different studies, which they looked at to draw their conclusions. Two of those studies had to do with dieting and weight loss.

From a press release:

“Four experiments show that when consumers encounter temptations that conflict with their long-term goals, one self-control mechanism is to exaggerate the negativity of the temptation as a way to resist, a process we call counteractive construal,” the researchers write.

For example, in one study, female participants were asked to estimate the calories in a cookie. Half the participants were told that they have the option of receiving the cookie as a complimentary gift for participation and half were not. The results showed that consumers with a strong dieting goal construed the cookie as having more calories and being more damaging to the attainment of their long-term goal of losing weight.

{snip}

In [another] study, female participants entered a room that either had posters depicting fit models or nature scenery. “Participants who were exposed to posters depicting fit models (goal-priming stimuli) were more likely to exaggerate the calories in a tempting drink that they expected to consume later on, and consequently consumed less when offered the drink,” the authors write.

The relevance to eating disorders is obvious, even when you ignore all of the stuff about weight loss. That's not what I find the most interesting. The key words that leaped off the page at me were "resisting temptation" and "exaggerate the threat." For many people, temptation is temptation. Someone who is predisposed to an eating disorder, however, may be much more likely to view temptation as a threat. You can add me to that category. People with AN in particular are prone to asceticism, which Wikipedia defines as "a lifestyle characterized by abstinence from various sorts of worldly pleasures (especially sexual activity and consumption of alcohol) often with the aim of pursuing religious and spiritual goals."

Want something even more ascetic that renouncing sex and booze? Renounce food. If these things weren't considered somehow "tempting"--read any nutrition advice about the holidays and you'll see what I mean--then they wouldn't need to be renounced. Many people with AN struggle with including pleasurable things in their lives. I'm not talking about pleasure from a night with your latest order from Good Vibes and a pair of AA batteries. I'm talking about the pleasure of relaxing in front of a fire, leaving the dishes until morning, going to a party even though you have a paper due the next day. Little things. I don't find them alluring as much as I find them anxiety-provoking, perhaps because they are so alluring to me. The thought of holding up a bank doesn't cause me anxiety because I have no desire to do so.

So there we have the part about "resisting temptation." Now we get to the part about "exaggerating the threat." The all work, no play work ethic of mine gets its oomph largely from my fears of what will happen if I play. How can I relax when there are stories that need researching and writing? How can I leave the dishes until morning when there might be a bug problem? How can I skip working on my paper, which could mean that I do horribly, fail the paper, fail the class, fail out of college, and wind up living in a cardboard box?

Like I said, "exaggerating the threat."

I'm a veteran calorie counter. When I'm wrong about the calories in something (which I occasionally am, although after 10 years, there's not a whole lot that I haven't already looked up), it's because I grossly over-estimated the number of calories in something, not an underestimate. An extra bite becomes 1000 extra calories in my mind. And when you consider that food is anxiety-provoking to people with eating disorders, there's already that tendency to exaggerate how awful, fattening, and massively portioned a food was.

Besides my food issues, I am also terrified of spiders. I've whacked off several roaches, millipedes, centipedes, and other bugs I didn't take that good of a look at. I don't like these bugs, but I can at least get rid of them with some shred of self-respect. Spiders are another matter entirely. Even a daddy long-legs seems huge to me. I see one and I scream like a girl. The other girls in my dorm always asked me to be on spider patrol because I was a "biology person." All I could think was that I use a microscope, not a fly swatter. Spiders seem massive to me- a literal interpretation of exaggerating the threat.

So when food seems far more threatening than it is tempting, it's easy to see how avoiding food would become almost instinctual.

One of the most profound things I learned in treatment for anorexia was how much the symptoms of my eating disorder (obsession with food, increased anxiety and insomnia, agitation, hyperactivity) were as much symptoms of starvation as they were symptoms of anorexia. Not that this made eating any easier--it didn't--but it helped put a context to all of the frightening thoughts and compulsions I was having. Eating seemed to make them worse, but only after a while did eating make them somewhat better.

Undernutrition may actually be at the core of many of the traits and symptoms researchers initially thought were caused by anorexia. Many people with anorexia are probably more obsessive, anxious, and perfectionistic than average; since these traits existed before the eating disorder, they aren't caused by undernutrition, but they sure can be exaggerated. Even just a quick read of Keys' starvation study indicates that many of the behavior changes brought about by semi-starvation can be significant. Many brain imaging studies of anorexia are performed after weight restoration and a period of recovery and normal eating because starvation has such profound effects on the brain.

There have been numerous studies that have reported on psychological changes that occur during refeeding (Konrad et al 2007), but two interesting studies appeared within the past week that seemed to emphasize the role of refeeding in the psychological recovery from EDs.

The first article was from the French journal Encephale, which looked at the relationship between social phobia, anorexia, and the stage of treatment (Coulon, Jeammet, and Godart, 2009). Because the journal is in French, I'm going to have to stick with the abstract, but the results were still interesting. Social phobia has been loosely associated with AN, but the researchers were trying to figure out whether the social phobia might be a by-product of malnutrition rather than an actual trait of the anorexia sufferer. In this sense, it's kind of the proverbial chicken-and-egg question: which came first, the undernutrition or the symptoms of the eating disorder?

And what did the researchers say about how stage of treatment in anorexia affected social phobia? They found a correlation between social phobia and symptoms of AN as well as "total clinical picture" of the patient, but no relationship between social phobia and nutritional status (as measured by BMI). The researchers concluded that "We therefore feel that a diagnosis of social phobia can only be confirmed after an acute state of AN, thus allowing for preferential treatments. Other studies must be conducted in order to continue to explore the links between social phobia and AN."

This doesn't preclude the pre-illness onset of social phobia--in fact, a 2004 study found that approximately one in five ED sufferers met the diagnostic criteria for social phobia before the onset of their disorder (Kaye et al, 2004). However, due to the eating disorder, social phobia can appear in a person who had no previous symptoms of the disorder. So is that social phobia a true, independent disorder, or is it related to undernutrition? This study says that social phobia might be related to undernutrition, but we don't know for sure yet.

The second study looked at the hypothesized relationship between anorexia and autism spectrum disorders (ASDs; Time Magazine had a good article earlier this year on the issue that I blogged about here). Specifically, the study looked at the difficulties people with AN have with respect to the emotional Theory of Mind (eToM), with understanding and interpreting others' emotions (Oldershaw et al, 2009). People with ASDs often have difficulty understanding other people's emotions, and the fact that AN sufferers also had difficulty with this seemed to be a neurological link between the two disorders.

The researchers compared a group of currently ill AN patients with both recovered AN patients and healthy controls, and found that the emotional deficits seen in acutely ill AN patients had essentially disappeared in the recovered AN patients. Furthermore, there were few differences in emotional tasks in recovered AN patients and healthy controls, which indicates that the emotional deficits are more related to the current state of undernutrition than they are a person's temperament.

Conclude the researchers:

These findings indicate almost complete normalization of emotion recognition ability as well as the restoration of eToM in recovered patients, despite the observation of difficulties in both domains in currently ill patients. Findings suggest that similarities between AN and ASD in poor eToM are restricted to the currently ill AN state and such difficulties in AN may be a factor of starvation.

However, other similarities between AN and ASDs remain, such as difficulties with set-shifting and impaired central coherence (i.e., you can't see the forest because of the trees) that seem to extend long beyond recovery. That, however, is its own blog post that will hopefully be up soon.

Last week, two interesting research papers were published that looked at the neurological origins of body image distortion in anorexia nervosa. And what researchers found was rather interesting.

The first article looked at not only how people with AN process body image, but it broke down that processing into two different steps: attitudes towards their body and how they experienced their own size (Mohr et al, 2009). Using fMRI, the researchers

"further demonstrated stronger activation of the insula and lateral prefrontal cortex during the satisfaction rating of thin self-images. This indicates a stronger emotional involvement when patients are presented with distorted images close to their own ideal body size. Patients also overestimated their own body size."

Furthermore, the researchers found a complex pattern of activation of the precuneus, an area of the brain that is thought to contain a sensory-based map of the body. Scientists hypothesized that people with AN have a deficit in their ability to pull up an accurate map of their bodies, leading to the body size overestimation so prevalent in AN.

I think it would be fascinating to compare fMRI scans of people with non-fat-phobic anorexia to those with AN and body dysmorphia. Perhaps this would help confirm that these different patterns are specific to body image and not related to anorexia in some other way.

The second paper looked at the role of the right parietal lobe in the formation of body image in people with AN (Nico et al, 2009). Part of the parietal lobe's job is to integrate sensory information from different points in the body, and stroke patients who have damaged right parietal lobes have difficulties with body representation and schema. Whereas people without AN and those with stroke damage to the left parietal lobe were able to estimate their bodies accurately, those with AN and stroke damage to the right parietal lobe were not. The researchers concluded that these results

"support the possibility for a neuropsychological component in the pathogenesis of anorexia, offering alternative approaches to treatment of the disorder."

Together, this research indicates that the body image difficulties in eating disorders go beyond seeing skinny models in magazines (though this doesn't help) and these neuropsychological differences play a role in the development of EDs.

I used to think that eating disorders were an extreme diet (this was a very long time ago). I thought there were people who didn't diet, people who dieted, and people with eating disorders, all arrayed on a nice little continuum, one blending seamlessly into the next. I've since learned that scholars are still considering this question, albeit in a more academic, less hand-waving sort of way.

Eating disorders are currently classified into three major categories: anorexia nervosa, bulimia nervosa, and eating disorder- not otherwise specified. What we don't know is whether these categories are just humanity's attempts to corral people with eating disorders into three categories, or if these are, in fact, three different eating disorders. Nor do we know if eating disorders are dimensional (ie, they exist along a continuum) or they are taxonic (ie, they have their own category, sort of like humans are a separate species from chimps. We don't have a human-chimp continuum, the behavior of several of my relatives notwithstanding). Perhaps a better analogy would be the difference between a light on a dimmer switch (dimensional model) and a light with an on/off switch (taxonic model). The methods for determining the difference between these use a lot of advanced mathematical models and some really fancy words--I'm not especially concerned in understanding precisely how the determination is made. Rather, I intend to look at whether we can make a distinction, and what that distinction is.

Like many new ideas in science, there is evidence in favor of both views. So let's start with a brief review of the evidence.

Eating disorders are dimensional

Thus far, one study has evidence that restricting anorexia exists along a continuum with "normal eating," although this study also found that bulimia and binge eating disorder do not exist along a continuum (Gleaves et al, 2000a). Perhaps one of the reason why restricting anorexia didn't appear quantitatively different from "normal eating" has to do with the prevalence of dieting behavior, which is more common than not in the college students surveyed in the study. In general, dieters have higher scores on the restraint/weight subsection of the EDI-2, but have similar psychopathology scores as non-dieters (Lowe et al, 1996), which really helps muddy the waters.

Interestingly, the Gleaves study found that the binge/purge subtype of anorexia was much closer to bulimia nervosa than the restricting subtype of anorexia, indicating that binge eating and purging is, in fact, taxometric, whereas restrictive behaviors are more dimensional.

When looking at nonbehavioral eating disorder symptoms (such as fear of fatness, obsession with food/calories), researchers failed to find any sort of eating disordered category, which would indicate that yes, indeed, eating disorders exist along a continuum (Tylka and Subich, 2003). A more recent study, building on this one, found that although eating disordered thoughts are common among people without clinical eating disorders, eating disordered behaviors are rather uncommon (Miller, Vaillancourt, and Hanna, 2009), which has implications on what, precisely, is measured on future studies.

Eating disorders are taxometric

The evidence for both binge eating disorder and bulimia nervosa seem to indicate that these disorders exist as their own categories; that is, either you have them or you don't (Lowe et al, 1996, Gleaves et al, 2000a, Gleaves et al, 2000b). Of course, a diagnosis is rarely as simple as one of those notes you likely received in sixth grade that said "Do you like me? Check yes or no."* There are lots of issues still to be worked out, not the least of which is where do we draw the line?

Perhaps one of the most interesting studies found a middle of the road for this discussion: some eating disorder symptoms existed on a continuum, and some, such as binge eating, fear of fatness/compensatory behaviors, and drive for extreme thinness, did not (Williamson et al, 2003).

Conclusion

At this point, the only consensus on the issue of eating disorder taxometry is the need for more research. Preliminary evidence suggests that bulimia and binge eating disorders are discrete symptoms; the evidence is less suggestive for restrictive anorexia. That being said, eating disordered thoughts are quite common, even if the behaviors are not, which could have significant implications on what is measured and studied in the future.

With the upcoming (and much-heralded) publication of the DSM-V in several years, these seemingly esoteric ideas could have a large impact on how we diagnose, treat, and prevent eating disorders.

Coming tomorrow: Classifying eating disorders, part two (What's temperament got to do with it?)

*Full disclosure: I neither sent nor received any of these notes.

There was a brief but interesting research article this past week on Interesting practitioners in training in empirically supported treatments, published in the Journal of Clinical Psychology. Despite a growing recognition of the importance of empirically supported treatments (otherwise known as evidence-based treatments), not all therapists are aware of these treatments or are willing and able to provide them. A good blog post from the Cleveland Center for Eating Disorders explains some of the reasons why.

Of course, all the training in the world isn't useful unless a therapist is interested in receiving that training. Speaking as someone with a research-oriented background, not a clinical one (nor even a psychological one), my first instinct would be to start by showing people the strength of the research base behind the treatment. What this paper found, however, is that most therapists responded more favorably to case studies rather than larger research studies.

Which, when you think about it, does make sense. Most therapists are more oriented towards people than they are towards large research studies (I'm the opposite, which helps explain why I'm not a therapist and never will be). This is neither good nor bad, it's just a general trend I've observed. Furthermore, case studies can provide more practical information in explaining how the therapy is carried out, how the patient responded, and what are some common pitfalls. This isn't to say that case studies should replace large research trials, just that they interest therapists more in empirically supported treatments.

For more information on empirically supported treatments, see both the Psychotherapy Brown Bag blog and this explanation from the American Psychological Association (they have information specifically on empirically supported treatments for eating disorders here).

Today's edition of Psychotherapy Brown Bag deals with the efficacy for Equine-Assisted Psychotherapy (EAP), specifically in the realm of eating disorders. What did the author, Mike Anestis, find?

EAP does not appear to be harmful, but there is no evidence that it is efficacious in the treatment of mental illnesses. There is a paucity of research on the topic and the research that exists is so full of flaws that it is actually rather remarkable that it was published in the first place. Nonetheless, fancy treatment centers charge outrageous fees to provide this service and make grandiose claims regarding efficacy. Just as we covered in our article on touch field therapy (TFT), such behavior is a prime marker of pseudoscience.

I don't doubt that riding horses is nice and fun and pleasant, but that doesn't mean that it helps treat eating disorders (or any other illness, for that matter). I find many things nice and fun and pleasant and even, in a sense, therapeutic, but that doesn't make it a treatment. I'm a big believer in the power of animals to make us feel better- my cat does it all the time. Nothing beats snuggling her in my lap or watching her silly antics. Spending time with her is often the highlight of my day. But it doesn't help treat my eating disorder. There's a big difference.

I've done some equine therapy while in treatment and maybe I'm just bitter, but I'm not sure what the point of it was. I get the theoretical premises upon which EAP stands (as summarized by Anestis):

•Improving non-verbal communication skills through interactions with a non-verbal creature
•Improvement of acceptance skills and emotional expression through the realization that a person can not make the horse do things it does not want to do (e.g., lift its hoof)
•Improved mood due to positive interactions with an animal
•Increased awareness of connection to nature through outdoor experiences

Which is all well and good, and no doubt there can be valuable lessons learned from equine therapy. (Although I must say that my cat has taught me everything and more that I need to know about point #2. The horse might be larger, but my cat has claws! :) ) Yet that still doesn't mean that EAP is an empirically-supported treatment. I find valuable lessons in coloring mandalas, in watching Grey's Anatomy and House, in crochet, in Sudoku puzzles. Not that these things can't be helpful, but it's a long stretch to say that these actually treat eating disorder symptoms.

I do realize that places like Remuda Ranch don't rely on horses alone for their treatment. But you better believe that EAP is one of the reasons they charge so much. Why pay extra for something that doesn't really work? Why not let your kid take horseback riding lessons or go trail riding once their ED symptoms have improved?

Anestis sums up his thoughts as follows:

I like the idea of using animals to make people feel better. In fact, Joye and I may one day train our sweet playful golden retriever to visit hospital patients in order to provide them with an added moment of happiness. In doing so, however, we will not be under the illusion that such an action would constitute therapy or treat mental illnesses. Our dog would simply provide a positive experience, which can impact mood and perhaps motivate an otherwise ambivalent individual to pursue the type of help capable of addressing the actual problem. When animal-assisted therapy is couched in these terms, it sounds wonderful. When it is presented as a stand alone treatment, however, that is a problem.

I don't think, however, that Aria would be very good at visiting hospital patients. Hiding under their beds and peeing, yes. Therapeutic, not so much.

Most humans like a sense of control in their world. Some of us (like me) like a sense of control more than others. And need for control stems from an inability tolerate uncertainty. I don't like surprises--not even in the form of presents. I don't like suspenseful movies. I don't like decisions hanging over my head. I like things to be clear and predictable.

I stumbled across a study that was published last year in the research journal Science titled "Lacking Control Increases Illusory Pattern Perception" by Jennifer Whitson and Adam Galinsky that addresses some of my favorite nouns bandied about in the eating disorder world: control. fear. superstition. rituals. A press release said that

[The researchers] showed that individuals who lacked control were more likely to see images that did not exist, perceive conspiracies, and develop superstitions.

"The less control people have over their lives, the more likely they are to try and regain control through mental gymnastics," said Galinsky. "Feelings of control are so important to people that a lack of control is inherently threatening. While some misperceptions can be bad or lead one astray, they're extremely common and most likely satisfy a deep and enduring psychological need."

According to Whitson, that psychological need is for control, and the ability to minimize uncertainty and predict beneficial courses of action. In situations where one has little control, the researchers proposed that an individual may believe that mysterious, unseen mechanisms are secretly at work. To test their theory, the researchers created a number of situations characterized by lack of control and then measured whether people saw a variety of illusory patterns.

"...People see false patterns in all types of data, imagining trends in stock markets, seeing faces in static, and detecting conspiracies between acquaintances. This suggests that lacking control leads to a visceral need for order – even imaginary order," said Whitson.

This reminds me a lot of how the need for control is discussed in ED treatment. Even though an eating disorder isn't about control, the need for control is the underlying theme of many eating disorder behaviors, whether it is controlling what is consumed, purged, exercised, or what have you. In so many personal accounts of eating disorders, I have heard statements saying something along the lines of "when everything else felt out of control, at least I could control my food."

But this research has made me look closer and think harder about what is actually going on. Stress is a frequent trigger of eating disorder onset and relapse, and one of the most stressful things is feeling like you have no control over your life. I've been there. It sucks. So maybe if the eating disorder wasn't "about" trying to control every aspect of my food intake, maybe this lack of control contributed to why I fell for the ED delusions hook, line, and sinker.

If I was like the people in Whitson's and Galinsky's study, then the times I was under stress, I would have been much more likely to assume that my decrease in food and increase in exercise helped make the situation resolve. It helped cement the superstitious beliefs that if I eat more than X calories or exercise less than Y hours or don't take at least Z laxatives, then all hell would break loose. Of course, nothing makes you feel more out of control than an eating disorder, so the beliefs and the need for pseudo-psychological order only increases. The "unseen mechanisms" proposed by the researchers was, in my case, the eating disorder. It simultaneously made the world go 'round, and also made my life cohere into a series of actions that I could understand and manage.

On the flipside, this research suggests that helping people gain control over their lives (which, in the case of EDs, would start with stopping symptoms) would decrease their endless mental gymnastics in trying to find a safe food, or a safe place to purge.

This has really made me re-think the role of control in eating disorders.