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."

Obsessive-compulsive disorder (OCD) is one of the most frequently diagnosed psychiatric disorders in people with eating disorders. It is known to make eating disorders more severe and harder to treat, leading to a longer time until remission is achieved. Recently, more and more researchers are beginning to recognize the significance of the overlap between EDs and OCD, and are trying to develop specific treatments targeted at this population.

A 2004 study by Walter Kaye and colleagues in the American Journal of Psychiatry measured how frequently anxiety disorders (OCD is a type of anxiety disorder) occurred in people with anorexia and bulimia. They found that two-thirds of the ED sufferers had been diagnosed with an anxiety disorder at some point in their life. In general, the onset of the anxiety disorder pre-dated the ED by several years. Of the people with an anxiety disorder, 41% had OCD and 20% had social phobia (social anxiety). The problem, then, is very significant.

The gold standard in treating OCD is a form of cognitive-behavioral therapy known as exposure and response prevention (ERP). You can read more about ERP here. The idea is relatively straightforward: You create a hierarchy of the things you're afraid of that would normally provoke a compulsion. For someone who is afraid of germs, something lower on the list would be touching an unused surgical mask. Higher up might be touching a doorknob at a doctor's office or being coughed on by someone with a cold. Together with a therapist, you would begin to expose yourself to these anxiety-provoking situations and then not engage in any compulsions (like hand-washing) to relieve the anxiety. The point of this is to learn to tolerate the anxiety and that you're not going to die if you happen to inhale a few germs.

Some researchers are beginning to use components of ERP to treat food fears in EDs, especially anorexia nervosa. In a 2011 study in the International Journal of Eating Disorders, researchers at Columbia University first outline a behavioral model for AN that is driven by anxiety and obsessionality (see figure below; the caption is copied from the paper).

Figure 1. Model of Anorexia Nervosa. Traits of high baseline anxiety and obsessionality interact with environmental factors such that patients develop maladaptive behaviors, including food avoidance, and rigid eating patterns (or dieting practices), and they experience high levels of anxiety around eating. These behaviors are interrelated in that rigid dieting leads to increased anxiety about food and vice versa. These behaviors result in a diet that is low fat (low energy density) and limited in variety. This, in turn, promotes weight loss. The low weight state feeds back on the baseline traits and leads to increased levels of anxiety and obsessionality.

Anxiety about eating more and gaining weight consistently interferes with weight gain in AN and with interrupting the binge/purge cycle in BN. The idea is that recovery cannot and will not occur unless these fears are addressed. In a 2012 review article in the European Eating Disorders Review, psychologists hypothesize that one of the reasons family-based treatment is successful for many adolescents is that it forces these exposures. Since the patients can't (theoretically) choose what to eat, they can't choose to avoid "scary" foods. Parents are also coached on how to help stop other food-related rituals

A study published earlier this week addressed the issue of treating OCD and EDs, this time in a residential setting. Published in Cognitive Behaviour Therapy, the researchers treated 56 individuals with AN, BN, or EDNOS in an eating disorder program specific for individuals with co-occurring OCD. Of these patients, 41% were diagnosed with AN, 25% with BN, and 34% with EDNOS. Rates and levels of depression and OCD did not appear to vary by diagnosis. After treatment, the researchers found a significant improvement on scores for OCD, depression, and eating disorders, as assessed by a variety of surveys and self-reports. Patients with AN also significantly increased their body weight.

Which is all well and good, but the problem is that this study (nor any others that I'm aware of) compared the treatment group to anything. Other studies have shown that treating an ED generally improves levels of depression and OCD. Was the improvement seen in this study due to regular eating and the prevention of binge eating and purging? What effect did being in a structured environment have? Would these results have been different if the patients weren't treated for OCD? What about if their OCD was treated and not their ED? I realize that actually conducting a research study in that last scenario would be unethical, especially in a group that qualifies for residential treatment, but it's something that should at least be considered in the discussion.

Another question the researchers didn't factor in was the use of psychotropic medication. Eighty-nine percent of patients were on some type of psychiatric medication; the authors said they didn't control for this in their analysis since only 7% started on medication during their treatment. But they didn't mention how many patients' medication was adjusted, increasing or decreasing dose, or changing types and brands of medication. These things can have a significant effect on OCD and depression symptoms (although a recent study indicated that no psychotropic medications appear to be effective for AN)

As well, one of the researchers is the medical director of the treatment center where the research was carried out. This makes me a little skeptical of the results as a matter of course.

The researchers concluded that "Simultaneous treatment of OCD and eating disorders using a multimodal approach that emphasizes ERP techniques for both OCD and eating disorders can be an effective treatment strategy for these complex cases." But how effective? Is it better? How much better? How long did the results last for? There was no follow-up on any of these patients. Improving in a program is great, but the rubber doesn't really hit the road until after discharge.

This study is a start, but it's a small start. Co-occurring EDs and OCD can be very difficult to treat, but many people do go on to develop healthy and productive lives. We desperately need more resarch into the subject, but we need to start making comparisons to help develop the best, most effective treatment possible.

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.

Most of you have probably noticed by now that it's Eating Disorders Awareness Week. For the first few days this week, my Facebook feed was inundated with message about loving your body and talking back to the media, and so on. It was like being at a high school pep rally, only about not wearing lipstick! and accepting our natural beauty! and loving our bodies!

I don't really like pep rallies, if for no other reason than I really don't do peppy all that well.

Rallying people and getting them motivated are great. Most of these war cries have to do with preventing eating disorders: that if we label digitally altered advertisements, we will decrease eating disorders. Or that people need to accept their natural sizes, which would eliminate eating disorders. They're nice thoughts, and they seem like really good ideas. It's why they have so much traction. People without eating disorders can relate to not liking how they look. They can relate to looking at beauty magazines and then feeling seriously ugly. They understand about dieting and wanting to be a Size Negative Eleventy Billion but not being able to lose those last XX pounds. Cindy Bulik calls this the "I just wanna look like a model" model of eating disorders.

The problem is that eating disorders aren't just extreme diets and treating them as such gets us nowhere. Writes Autumn Whitefield-Madrano, a recovering (?) eating disorder patient:

I just know that by the time I was discharged from Renfrew, I’d finally begun to learn that my dissatisfaction with my body wasn’t causing my eating disorder; it was merely a symptom of my disease, like restricting my food intake or binge eating...I’d begun to understand that loving my body wasn’t the point. The point wasn’t even to like it. The point was to learn how to eat.

I personally find body image--how the brain figures out what we look like--a fascinating neuroscientific and philosophical issue. My own body image issues long predated my eating disorder, but they didn't have anything to do with lipstick or models.My brain had a hiccup in figuring out what size I really was, likely due to problems in the insula and somatosensory cortex. Ridiculously altered images don't help, but they weren't a cause.

Others take a different approach towards eating disorders prevention. If we can educate people about how dangerous and pointless eating disorders are, then maybe people won't start. It's an attitude I had myself for a while, and the well-meaning philosophy feeds into tell-all newspaper articles and discussions about just how few lettuce leaves you survived on at your worst.

I never ceases to astound me just how many people give a shit about that sort of thing.

Except that this type of thinking essentially posits that eating disorders are choices, or voluntary behaviors. Perhaps that first step can be, I don't know. The problem is that most people who take that first step don't think they're going to develop an eating disorder as a result. So telling them that eating disorders are dangerous is kind of pointless, since they're not going to get an eating disorder from adding a little bit to their athletic training or cutting out junk food or whatever. By the time they have an eating disorder, it's too late.

To wit: a recent study on weight history in bulimia was just published, and researchers found that women suffering from bulimia ultimately gained weight as the result of their disorder. The Atlantic magazine wrote:

"Most patients lose a lot of weight as part of developing this disorder, and all dedicate significant effort, including the use of extreme behaviors, to prevent weight gain," said researcher Jena Shaw. "In spite of this, we found that most women also regain a lot of weight while they have bulimia," she continues. Maybe tell that to those kids with their pro-bulimia "ana-mia" Tumblrs?

{{Emphasis mine.}}

Nice thought, but it probably won't work to actually prevent an eating disorder. It's like telling someone who's sad to cheer up lest they get depression, or working to prevent bad moods everywhere! (Like pep rallies, unbridled optimism also makes me stabby, so I'm not sure I could tolerate this world for long...)

I'm not against the prevention of eating disorders, I'm just not sure that we have any clue how to do it yet.

I'm spluttering not so much at this article about insurance refusing to cover bulimia treatment (though the situation is very much splutter-worthy), but at the comments.

Generally, I don't read the comments on news articles mostly because they're either from extremist wingnuts, they're irrelevant, or people use the anonymity of the web to act like immature jackasses.  But I started reading the comments on this article, and my eyes just saw red.  I've gotten used to a lot of the misconceptions about eating disorders ("Just eat a sandwich!"  As if that hadn't occurred to me...) and although they're annoying, I understand that much of them stem from a lack of knowledge rather than sheer idiocy.  That is, I have hope that this person will one day understand EDs a little better once they have more knowledge.

These comments, however, are the epitome of sheer idiocy.  Some examples:

Blue Cross/Blue Shield is my insurance carrier as well. I will call and support them in this decision and I hope many more call and support this decision. I don't want to pay for her care. She is an adult, she needs to take care of herself. I'm glad this has been on the news. It brings awareness to many of us, of the crazy things people try to get insurance companies to pay for. No wonder this country is in a health care crisis. If we all get a disease then we can all be on easy street. WHATEVER

They don't help many child genetic issues either. The disabled children in this country and the Veterans in this country can't even get the medical help they need. So, why does this family feel that their daughter's condition is worthy of help? As far as I am concerned they can pay for it out of there pocket. I have to pay for "most" of my disabled child's medical bills, because insurance won't pay them. Do you see me ranting on tv and picketing the insurance company? No!!!

Or

Let her parents support her! Why should the insurance company pay. In the end all of us that have insurance with BCBS will be contributing to paying for her care. I too am going to call them tomorrow and agree with their decision to not pay for her care. My grandparents need medical help,they have cancer, the insurance company don't pay all of their bills. They act responsible and pay their bills, they don't go picket the BCBS office. They pay for their own home care.

The logic is so bad it's astounding.  Yes, getting sick drives up health care costs.  We will all get sick and it will cost money to get it treated.  Unless you have a way to prevent all illness (and something tells me if you're this blatantly stupid, you don't have the extra neocortex to come up with something so groundbreaking), then we're going to get sick and need insurance.  Any questions?

Also, I think some of these people have picket envy.  If you're pissed off, go picket.  It's your right.  You're allowed.  But don't get pissed because you can't/don't/won't take such a stand.

I just end up incensed when people (some of whom are in my family) see an eating disorder as the self-indulgence of a pampered kid.  I was exercising for hours a day on a broken foot--that's not being pampered.  Something primal in my brain was driving that, something that can't be explained by wanting to stay on my parent's health insurance policy (which wouldn't have happened because I was 28).  If that was the case, the curing an eating disorder would be as easy as refusing people with EDs health insurance.  It has happened to me (I am, literally, uninsurable), and I didn't spontaneously recover once that occurred to me.

I know I shouldn't let the little bastards get to me.  There were supportive comments on there, too.  I know most people try to understand.  But every now and again, the ignorance just astounds me.  I don't wish an eating disorder on anyone, but sometimes, I do wish these people would be able to experience an eating disorder from the inside before they open their gaping, ignorant maws and spew forth utter crap.

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.

As I promised two days ago, here are my thoughts on the other changes made to the DSM. I blogged previously about my thoughts related to the changes made about anorexia nervosa, so now it's onto the other diagnoses.

Bulimia Nervosa

The changes to the BN diagnosis were twofold:

• the frequency of binge eating and purging was decreased from 2x/week for 3 months to 1x/week for three months


• the "non-purging" BN subtype was eliminated, and merged with Binge Eating Disorder

The first criteria is pretty straightforward and there is quite a bit of evidence to indicate that so-called "sub-threshold" bulimia is just as severe as "threshold" bulimia in the DSM-IV (Krug et al, 2008; Wilson and Sysko, 2009). This change isn't anything I have any desire to argue with.

The second criteria is more problematic. The drafters of the ED criteria for DSM-V had this rationale about the change:

DSM-IV requires that sub-type (purging or non-purging) be specified. A literature review indicated that the non-purging subtype had received relatively little attention, and the available data suggested that individuals with this subtype more closely resemble individuals with Binge Eating Disorder. In addition, precisely how to define non-purging inappropriate behaviors (e.g., fasting or excessive exercise) is unclear.

Deletion of this subtype is recommended. This also requires rewording of Criterion B.

Criterion B specifies "inappropriate compensatory behaviors," and these behaviors would be limited to self-induced vomiting, and misuse of laxatives and/or diuretics. To some extent, I see the difficulties in defining fasting or excessive exercise- it isn't clear. But my next question would be then to define the "misuse" of laxatives and diuretics. So if you binge and then you can't take a crap and you swallow a few pills, is that misuse? What if the box says take two to four pills, and you always take four because you're convinced that any less wouldn't get the food out. Is that misuse? You're following the directions on the box, after all. If they specified "use" of laxatives and diuretics to specifically try and "undo" a binge, then I wouldn't probably be so prickly. It's clear that it's a purging behavior. But misuse? If the idea is to get rid of unclear definitions, I'm not entirely sure they did that.

My other question is this: I thought fasting and exercise were kind of considered forms of purging. I'm not sure what the distinction is--does purging have to involve your mouth or your butt? Sorry to be kind of crass, but I'm still trying to figure that one out. It's one thing to remove the subtypes and just create a "bulimia nervosa" definition that encompasses both purging and non-purging types, but I'm not positive on the wisdom of removing fasting and excessive exercise from the BN criteria.

The DSM-V draft criteria cited a study titled "The Validity and Utility of Subtyping Bulimia Nervosa," which came to the following conclusions:

Another possible reason for the lack of data on individuals with BN-NP may be a problem in diagnosing these subjects. Individuals who would qualify for the diagnosis BN-NP may go unnoticed or be wrongly diagnosed as BED or ED-NOS as a result of incomplete assessment of nonpurging compensatory behaviors. Both dieting and exercising are common in the general population, and are not necessarily pathological. There is no clear criterion to decide at what point the amount of exercising and dieting exceeds a cut-off point and becomes abnormal. This does not mean that nonpurging compensatory behaviors are clinically irrelevant. A number of studies have provided information that both purging and nonpurging compensatory behaviors are important clinical markers, for example, they both have high rates of comorbidity; their frequency is associated with severe maladaptive core beliefs and they are associated with impaired social functioning. The lack of clear definitions of nonpurging compensatory behaviors combined with their clinical relevance highlights the need for better diagnostic criteria.

Although the number of subjects with BN-NP [non-purging bulimia nervosa] is generally lower than that of BN-P [purging bulimia] and BED, in some studies the rates are comparable to, or in favor of, BN-NP, notably for three of the five general population studies. This may be a result of the more standard use of (semi-) structured diagnostic interviews in this type of study, in which the presence of nonpurging compensatory behaviors is routinely checked. Again, this calls for increased attention to the formulation of clear and easy to apply diagnostic criteria for nonpurging compensatory behaviors.

The study called for one of three possible solutions to this subtyping issue:

1. Maintain the current situation by keeping BN-NP as a subtype separate from BN-P as in DSM-IV, that is, a distinction between purging and nonpurging types of compensatory behavior in people who binge eat.


2. Eliminate nonpurging compensatory behavior as a diagnostic criterion. Individuals
   receiving a diagnosis of BN-NP in DSM-IV would be designated as having BED.


3. Inclusion of BN-NP in a broad BN category, as suggested by Walsh and Sysko, where a combination of binge eating with only nonpurging forms of compensatory behavior would be considered an atypical form. This would require a clear definition of the normal/abnormal boundaries of food restriction and exercising.

Obviously, the decision was made in favor of option 2.

How the specific vagaries of diagnosis will affect treatment remains to be seen. The irony is that most treatments for BED recommend physical activity--which is fine, but not for someone who uses exercise as a compensatory behavior. The debate isn't settled, and I'm not sure what I would do myself if I got to have the DSM Magic Wand.

Binge Eating Disorder

Binge eating disorder was included, which was a HUGE victory (no pun intended). BED is been fairly well defined for quite some time, and there are specific treatments that can help people struggling with binge eating.

The frequency of binge eating was specified at 1x/week for three months to make it more in line with the BN diagnosis. This seemingly low threshold for binge frequency has gotten some people up in arms. Writes psychiatrist Allen Frances in an article titled "Opening Pandora's Box":

Binge Eating Disorder will have a rate in the general population (estimated at 6%) and this will probably become much higher when the diagnosis becomes popular and is made in primary care settings. The tens of millions of people who binge eat once a week for 3 months would suddenly have a “mental disorder”― subjecting them to stigma and medications with unproven efficacy.

This is certainly a valid concern (a diagnosis should adequately capture all people who are ill with a disorder and none of those who aren't), but just because a diagnosis is more common doesn't mean it's not real. Also, the problems with people being subjected to medication seems more of a problem with our messed-up health care system and non-specialists making rather specialized diagnoses (I wouldn't want my cardiologist trying to diagnose my foot problem) than with the actual diagnostic criteria.

If the criteria for BED was just one binge a week for three months, I'd be much more willing to concede Dr. Frances' point. However, there are other criteria for BED that include feeling overly guilty or disgusted with oneself; the feeling of not being able to stop eating; feeling depressed afterwards; etc. Occasional overeating is unlikely to happen alone and result in "marked distress."

Still, Frances' overall argument is interesting and timely and well worth reading.

Purging Disorder

Rachel at The F Word pointed out the lack of formal inclusion of purging disorder in the DSM-V by highlighting this paragraph from the EDNOS section:

The work group is considering whether it may be useful and appropriate to describe other eating problems (such as purging disorder–recurrent purging in the absence of binge eating, and night eating syndrome) as conditions that may be the focus of clinical attention. Measures of severity would be required, and these conditions might be listed in an Appendix of DSM-5. If these recommendations are accepted, the examples in Eating Disorder Not Otherwise Specified will be changed accordingly.

I'm not surprised that purging disorder didn't make it in as a stand-alone diagnosis, not because the data isn't good--it is--but that it's rather new. Rachel has a whole post devoted to purging disorder that is well worth reading, and you can find more studies on purging disorder here.

Earlier this week on Twitter (do you follow ED Bites on Twitter? You know you want to...), I ran across an interesting article about why some antidepressants don't work in some patients. The article was published last week in the research journal Neuron and is titled "5-HT1A Autoreceptor Levels Determine Vulnerability to Stress and Response to Antidepressants." (Clicking the link will take you to the free full-text of the article.) I'll let the opening of the article's Science Daily press release explain the research for me:

An excess of one type of serotonin receptor in the center of the brain may explain why antidepressants fail to relieve symptoms of depression for 50 percent of patients, a new study from researchers at Columbia University Medical Center shows.

...Most antidepressants -- including the popular SSRIs -- work by increasing the amount of serotonin made by cells -- called raphe neurons -- deep in the middle of the brain. Serotonin relieves symptoms of depression when it is shipped to other brain regions.

But too many serotonin receptors of the 1A type on the raphe neurons sets up a negative feedback loop that reduces the production of serotonin, Dr. Hen and his colleagues discovered. "The more antidepressants try to increase serotonin production, the less serotonin the neurons actually produce, and behavior in mice does not change," Dr. Hen says.

Seeing as anti-depressant therapy hasn't shown much promise in the treatment of anorexia nervosa (although it does appear to help treat co-morbid conditions like depression and anxiety), this research could help with the development of new treatments for AN. It also seemed like a good a time as any to discuss the links between serotonin levels and eating disorders. In a 2005 review article, titled "Serotonin alterations in anorexia and bulimia nervosa," Walter Kaye wrote that people with either anorexia and/or bulimia showed alterations of brain functioning in specific neural areas:

Importantly, such disturbances are present when subjects are ill and persist after recovery, suggesting that these may be traits that are independent of the state of the illness. Emerging data point to a dysregulation of serotonin pathways in cortical and limbic structures that may be related to anxiety, behavioral inhibition, and body image distortions...Alterations of these circuits may affect mood and impulse control as well as the motivating and hedonic aspects of feeding behavior. Such imaging studies may offer insights into new pharmacology and psychotherapy approaches.

The serotonin/anorexia connection has been researched over the years (searching PubMed for "serotonin anorexia" gives you over 700 results), and the most recent thinking goes something like this. People with anorexia are generally thought to have unusually high levels of serotonin in their brains, and high levels of brain serotonin have been linked to anxiety and obsessionality. An old BBC article titled "Genetic clues to eating disorders" has a quote from Janet Treasure that explains some of the link:

People with high levels of serotonin are prone to anxiety. Dr Janet Treasure, director of the eating disorders unit at the Maudsley, believes this could be behind anorexic patients' ability to suppress appetite. She said: "In anorexia nervosa the drive to eat can be inhibited, but we know that in normal people who are starved they will kill each other and do all sorts of morally repugnant things, and eat all sorts of foodstuffs that you wouldn't normally touch.

"Yet that doesn't happen in anorexia nervosa, so there's some aspect of the appetite system that isn't working."

The unit looked at the biology of stress mechanisms, in particular the fight or flight response. This is where the body prepares itself for action when confronted by a stressful situation. Heart rate and blood pressure rise and two of what are usually humans' highest priorities, eating and reproducing, are put on hold. It is possible that anorexic people are chronically in an acute state of stress reaction - they are constantly in a fight or flight state of mind.

And by restricting food intake, people with anorexia can lower the amount of serotonin their bodies can make (serotonin is ultimately derived from the essential amino acid tryptophan). This actually makes people with anorexia feel better. However, the brain begins to sense the decreased serotonin production and tries to maintain homeostasis by increasing the number of serotonin receptors. Thus the brain is back at Square One, as it is producing less serotonin but is using the decreased amount much more efficiently. So restricting doesn't feel as good, and the (obvious!) solution is to eat even less. And thus that negative cycle is born and the anorexic becomes trapped by their own brain chemistry.

Refeeding would then increase the amount of serotonin in the brain before the brain has a chance to decrease the number of serotonin receptors. This could be the neurological equivalent of All Hell Breaking Loose and could very well explain why refeeding is so distressing, although I don't think there has been any formal research done on the subject.

In bulimia, the serotonin problem is reversed. People with BN appear to have much lower than average levels of serotonin in the brain, which may be temporarily increased by binge eating.* Purging increases levels of vasopressin, which can have a euphoric and sedating effect, thus making the binge/purge cycle addictive much in the same way that starvation becomes addictive in AN. The chronic low levels of serotonin in BN also explain why SSRIs can be effective at reducing the urges to binge and purge.

Of course, plenty of people cross over from anorexia to bulimia, and I haven't the slightest idea of how serotonin might affect that crossover. So many brain systems are thrown out of whack during an ED that I don't know an exact answer will ever be found.

*The story is, as usual, a little more complicated than this, but the basic idea is the same.

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.

This week's Science Times in the NY Times featured a profile of psychologist Russel Hurlburt, who studies the inner experiences of people with mental illness. For many mental illnesses, the DSM spells out the symptoms that people have, but it doesn't really describe what it's like to have a particular illness. For that matter, knowing what cancer is and how to treat it isn't the same as knowing what it's like to have cancer and undergo treatment.

From the profile:

After hundreds of introspective interviews, Dr. Hurlburt still hesitates to generalize from his findings. But he has observed that the basic makeup of inner life varies substantially from person to person.

“My research says that there are a lot of people who don’t ever naturally form images, and then there are other people who form very florid, high-fidelity, Technicolor, moving images,” he said. Some people have inner lives dominated by speech, body sensations or emotions, he said, and yet others by “unsymbolized thinking” that can take the form of wordless questions like, “Should I have the ham sandwich or the roast beef?”

In a 2006 book, “Exploring Inner Experience,” Dr. Hurlburt suggests that these differences may be linked to personality and behavior. Inner speakers tend to be more confident, for example, and those who think in pictures tend to have trouble empathizing with others.

Differences in thinking style may also help explain some aspects of mental illness. In studies conducted with Sharon Jones-Forrester and Stephanie Doucette, Dr. Hurlburt found that bulimic women experienced a clutter of simultaneous thoughts that could often be cleared by purging.

Which makes sense to me. If you want to consider exercise a form of purging, I can definitely attest that purging slowed my racing thoughts and really calmed me down. Purging (granted, I have purged in more ways than exercise, but that was my most common and recent form of purging) was almost like dissociating. It's not exactly the same, and I wasn't dissociated while exercising/purging, BUT my brain also felt very separate from my body, almost like it was observing me running or pedaling or whatever.

I tried looking for any publications by Jones-Forrester and Doucette, but it appears that their work on the inner experiences of people with bulimia consisted mainly of doctoral dissertations under Dr. Hulburt. I found the abstract of Jones-Forrester's thesis, which reads:

Inner experience is of crucial importance in bulimia---clearly something experiential leads individuals to binge or purge. We used Descriptive Experience Sampling (DES) to examine the inner experience of bulimia in 5 participants, replicating Doucette (1992). Our participants' inner experiences were largely consistent with Doucette's but were substantially different from what is assumed by the non-DES literature: our bulimic participants had a consistent fragmentation of attention, hypersensitivity to the sensory aspects of experience, affect that is poorly differentiated and often confused with cognition, and a striking lack of cognition overall. These results suggest that DES can be a powerful tool to challenge the assumptions of the extant literature and to expand our understanding of bulimia.

Hurlburt cited the research of Doucette in his 1993 book "Sampling Inner Experience in Disturbed Affect," sections of which are available on Google Books. From this book:

Multiple Inner Experience is the simultaneous occurrence of a few or many separable, identifiable inner happenings, all taking place in inner experience at the moment of the beep. One of the most striking findings in our study of bulimics was that Multiple Inner Experience was a frequent characteristic of the inner experience of all our bulimia subjects. This is in sharp contrast to the findings of other researchers sampling non-bulimic populations, where the phenomenon of Multiple Inner Experience occurs occasionally but is rare (an exception is the example of Borderline Personality described in Chapter 14). In contrast with other subjects, however, Multiple Inner Experience was the rule, rather than the exception, among our bulimics: the frequency ranged from 40% to 100% within our individual bulimic subjects.

It was also the case that, for our bulimic subjects, the presence of Multiple Inner Experience was directly related to the degree of bulimic symptoms: the more actively bulimic the subject, the more multiple the inner experience. This was true both when considering the percentage of a subject's samples containing Multiple Inner Experience (the more actively bulimic, the higher the percentage) and also when considering the multiplicity of experience at any given sample (the more actively bulimic, the higher the number of separate experiences which were reported to be simultaneously occurring at any one beep).

{snip}

A third characteristic experienced by our bulimic subjects was the relatively blurred distinction between thought and feeling. Our bulimics frequently seemed to "think their feelings" or "feel their thoughts." By contrast, most normal subjects in our sampling were very clear about the distinction between thinking and feeling. Even on those occasions where they have difficulty providing the experiential details of a thought...most non-bulimic subjects have no doubt that the thought is a "cognitive" or "mental" experience; the same is true for affective experiences. An exception is our anxious subjects (see Chapter 13), who also at times had difficulty distinguishing between affect and cognition.

{snip}

The intensity of the urge to purge seemed more related to the heightened multiplicity of thoughts and feelings than to the content of food or weight.

(Emphasis mine)

I find this work of Hurlburt, Doucette, and Jones-Forrester to be absolutely fascinating, and I really wish there was more peer-reviewed research on the subject. Still, this work may help fill in the gaps between what we know about bulimia and how BN is experienced.

In a well-thought editorial in the American Journal of Psychiatry, my homeboy Walt Kaye has written an editorial on eating disorders titled "Eating Disorders: Hope Despite Mortal Risk." Besides presenting good information, what I especially loved about this piece was how Kaye balanced the severity of EDs and their potential deadly nature with hope for recovery.

Kaye explains the "vicious circle" of ED behaviors with a nice diagram (below) and this summary:

Childhood personality and temperament traits, which tend to be relatively mild, appear to contribute to a vulnerability to development of an eating disorder (7). Such traits may become intensified during adolescence as a consequence of the effects of multiple factors, such as puberty and gonadal steroids, development, stress, and cultural influences. For anorexia nervosa, there is a dysphoria-reducing character to dietary restraint. In contrast, for bulimia nervosa, overeating is thought to relieve negative mood states. But chronic pathological eating leads to neurobiological changes that increase denial, rigidity, depression, anxiety, and other core traits, so that patients often enter a vicious circle. This results in a out-of-control downward spiral whereby a significant proportion of patients develop a chronic illness or die. Fortunately, a substantial portion of those with anorexia nervosa and bulimia nervosa recover by their early to mid-20s, although mild to moderate degrees of temperament and personality traits persist, often with positive attributes.

Since these personality traits usually existed before the onset of the eating disorder, they likely persist after recovery. The key, says Kaye, is to use these traits for good instead of evil. For many individuals, learning to guide their innate personalities is a major task for ongoing recovery.

But receiving effective treatment in order to reach a lasting recovery is often difficult. Access to care--whether financial, geographical, or otherwise limited--is surprisingly low in many places. Denial of treatment by insurance companies (in the US) poses a major limitation to how effectively a person can be treated.

Writes Kaye:

It is important to emphasize that these individuals—and their families—suffer for many years while symptomatic and, as the Crow et al. study (3) suggests, may be at risk of dying during this period of illness. Still, it is critical that insurance providers recognize that for many individuals, anorexia nervosa and bulimia nervosa do not constitute a black hole of endless treatment costs. In fact, appropriate treatment may keep people alive and healthy during the years that they are symptomatic. Such treatment counteracts the out-of-control spiral, minimizes medical complications, and presumably increases the likelihood of a good outcome. Moreover, many families get burned out during the seemingly endless struggles during the ill state. To prevent families from giving up, it is important to explain to them that many individuals with eating disorders do get better, but only after many years.

One of the next major tasks of researchers is to find ways to decrease the length of time to recovery and reduce the chronicity and mortality rates of eating disorders.

I found two related stories on exercise bulimia in my news feed today, and although they weren't glaringly inaccurate, there were some aspects I found mighty amusing (but not in a funny way).

The two stories were: Emerging Eating Disorder- Exercise Bulimia, and San Diego Clinic Helps Exercise Bulimics. The first aired on the CBS "Early Show," and the second appeared to be from their San Diego syndicate.

First of all, exercise bulimia isn't an "emerging" disorder. It's a fairly new name for a really old phenomenon. When the first clinical descriptions of anorexia were written in the 1870s, doctors noted the patients' hyperactivity in the face of starvation. Compulsive exercise has long been a feature of eating disorders, and our current cultural obsession to try and burn off excess calories through exercise only feeds this mentality and normalizes the disorder.

Secondly, a link on "related articles" on the first piece linked to an item called "Want to Lose Weight? You Gotta Work Out."

I mean, Holy Irony, Batman!

Also, very 80s graphic they have going there. Yikes.

Thirdly, the text about the San Diego clinic opened with the following: For most of us, hitting the gym is a necessary evil to keep those extra pounds at bay.

*headdesk*

This just confirms that so many people just don't get it. The mentality that exercise is all about weight loss and that more exercise is better because it means more weight loss and dedication only fuels the problem. During my exercise addiction, no one ever asked if I had better things to do than live in my rank sports bra. I get that these articles are meant to be helpful, but they also continue the subtle misinformation about the nature of these disorders.

Two new research studies out this week have delved more into the issue surrounding eating disorders in midlife (I've written on the subject before here).

One study looked at factors associated with disordered eating and body image dissatisfaction in middle aged women. It wasn't exceptionally mind-blowing research, but it did seem to uphold that many of the traits that put people at risk for EDs earlier in life still put people at higher risk later in life. What traits? Things like placing a high importance on appearance and function, poor self care, and lower cognitive reappraisal. These women also had higher BMIs than women without eating disorders.

The cognitive reappraisal in particular interested me, because this particular study looked at how these women were able to reframe changes in appearance due to aging. So rather than looking in the mirror at their gray hair and crow's feet and thinking "I'm an old hag," a woman could look at the same features and think of them of signs of a life well-lived. It strikes me that these difficulties echo difficulties with set-shifting that have been previously documented in people with eating disorders.

The other study looks at the 20-year outcome of both bulimia and EDNOS, beginning at an average age of 20 years, and ending at an average age of 40 years. Approximately three out of every four people who had BN at the beginning of the study had reached remission by the end of the study. Meaning, of course, that 25% of people with BN fail to significantly improve (though "remission" was not formally defined in the abstract). The authors said this:

Eating disorder point prevalence declined in women but not men from late adolescence to mid-life.Despite patterns of improvement in women, 4.5% reported a clinically significant eating disorder at mid-life, suggesting the need for more research on potential risk factors in this age group, such as pressures for women to maintain a youthful appearance.

And, I might add, research needs to focus on developing better treatments for BN and determining ways to help people stick with treatment.

It would be interesting to see how these numbers compared to rates of midlife EDs twenty years ago. Unfortunately, we don't really have this information. It seems that our culture's emphasis on beauty and youthfulness (or beauty as youthfulness) only helps perpetuate the factors that make people--especially women--vulnerable to EDs in the first place.

Disregard the sensationalistic title and check out this wonderful essay called "I was a baby bulimic: A food critic comes to terms with his appetite," by Frank Bruni.

What struck me, besides the descriptions of bulimia by a male in the early 1980s, was how early in his life the overeating and purging started, and how it appeared to be an echo of many of his mother's conflicts with food.

What also struck me was his haunting descriptions of his illness and how closely it echoed my own frenzied episodes of binge eating and purging:

To be a successful bulimic, you need to have a firm handle on the bathrooms in your life: their proximity to where you’re eating; the amount of privacy they offer; whether — if they’re public bathrooms with more than one stall — you can hear the door swing open and the footfall of a visitor with enough advance notice to stop what you’re doing and keep from being found out.

You need to be conscious of time. There’s no such thing as bulimia on the fly; a span of at least 10 minutes in the bathroom is optimal, because you may need 5 of them to linger at the sink, splash cold water on your face and let the redness in it die down. You should always carry a toothbrush and toothpaste, integral to eliminating telltale signs of your transgression and to rejoining polite society without any offense to it. Bulimia is a logistical and tactical challenge as much as anything else. It demands planning.

It is interesting, of course, that Bruni wound up as a food critic. This essay was adapted from an upcoming autobiography titled "Born Round: The Secret History of a Full-Time Eater," which has now gone on my reading list.

Were you struck by anything in particular in the article? What could you relate to? What didn't you like? Share away in the comments section!

This presentation by Walter Kaye was filmed in March of 2001, before I was even diagnosed with my eating disorder, yet no one ever told me about it or mentioned it. It explains EDs so clearly and succinctly, without blame or psychobabble, that I am astounded no one bothered to let me know this great information.

The New Biology of Anorexia and Bulimia Nervosa: Does Dieting Help People with Eating Disorders Fit Into Their Genes?

You'll need QuickTime to view- I didn't have much luck, so let me know if you can see it.

Otherwise, just click here to view the slides. There's one gratuitous skinny person picture, but it's not too bad.

Then again, I don't know why I'm surprised no one told me about so much of the great information out there. I did find it, yes, which makes me lucky enough to be tech savvy to know how to search and inquisitive enough to go looking. But I shouldn't be the person doing the research to learn all about my own illness. I wish someone out there had told me such great information, right from the get go.

Am I bitter? Maybe.
Has it fueled my passion? You better believe it.

A powerful music video of the life of Shelby Starner, a young musician who died from bulimia in 2003.



(Thanks, Greg, for alerting me to this!)

I read a sad story in this morning's Washington Post, about a family struggling to understand their 19-year-old daughter's death from bulimia, six years ago. The article was powerfully written and illustrates how deadly eating disorders are. It also illuminated how we not only need better treatment, but need more treatment providers to be aware of life-saving therapies like the Maudsley approach.

My heart goes out to the Siskins and what bulimia has taken from their family.

But what floored me the most, what left me utterly speechless and appalled, were the comments left. I blog a lot about debunking the stereotypes of eating disorders, of how they are real mental illnesses, and although I get frustrated at times, I operate within a community that understands the seriousness of these illnesses. And they are illnesses.

My security within this insulated community was sideswiped when I read that some people consider bulimia "a hybrid of the mortal sins of gluttony and pride," or that you can "never get over" an eating disorder. That too much TV causes eating disorders, no it's magazines, or maybe it's just "society and it's evil media machine is definitely to blame."

Or I read that some people think "Their disease is the sneakiest, most underhanded. I am sick of the sympathy they get when they seek to deceive constantly. The pain they're in is no different than the pain an obese person is in. But you coddle them. If we TRULY examined the hypocrisy here, you'd see that you have a horrific double standard."

We need less finger pointing and more research, more answers, more treatments. We need to stop blaming "society" and look more at biology. We need to stop treating eating disorders and recovery as a simple choice. We need more compassion towards the people who suffer and die from eating disorders.

I don't have much time right now, but I couldn't let this one pass by without making immediate comment: a new decade-long study has just been released that tracked bulimic symptomatology among adolescent girls of varying racial and socioeconomic groups. And the results blow any notion that eating disorders are a rich, white girl's disease straight out of the water.

In a survey of 2300 girls from around the country, a team of researchers led by USC economist Michelle Goeree and economist John Ham of the University of Maryland, found that

"girls who are African American are 50 percent more likely than girls who are white to be bulimic, the researchers found, and girls from families in the lowest income bracket studied are 153 percent more likely to be bulimic than girls from the highest income bracket."

Furthermore, African American girls measured higher on a clinical index of bulimia severity than their white counterparts. Overall, 2.2% of the girls had clinical bulimia nervosa, equivalent to other population estimates.

Many measures of eating disorders depend on rates of diagnosis; however, given the secretive and shameful elements of eating disorders, combined with mental health stigma and the expense of care, the population of sufferers presenting for treatment is not necessarily the same as the total population of people suffering from bulimia. This research, which surveyed girls annually and asked questions relating to ED symptoms, body image, and depression, paints a much more heterogeneous picture of sufferers than those that appear in the popular media.

"The results illustrate the importance of having objective information on behavior rather than relying solely on data on diagnoses," Ham says.

According to Goeree, past research has over-relied on hospital admission data, creating a "sample selection bias" that overlooks those who exhibit bulimic behavior but do not receive — or have the means to receive — professional help.

"One explanation is straightforward: Girls with an eating disorder who are African American or come from low-income families are much less likely to be diagnosed. Who goes to the hospital? Those who have insurance. Who tends to have insurance? Wealthier, better-educated people," Goeree says, noting that another part of the difference may be due to parents' sensitivity to bulimic behaviors.

The findings also affect educational spending: "What we thought was that bulimia affects high income, high education white women. And, if that's the case, then you should try to tailor educational programs — because education is expensive — to the group that it will help the most," Goeree explains. "Now we're finding that it's really important to reach a completely different group than we thought."

And these results have implications for treatment.

"Based on their findings about the persistence of bulimic behavior and who is afflicted, the researchers argue that bulimia, which is currently classified as a disorder, would perhaps be more accurately described — and treated — as an addiction. As with drug and alcohol addictions, this would mean more federal, state and local treatment programs and fewer out-of-pocket insurance costs."

The summary didn't show what, if any, correlations were found between measures of depression, body image dissatisfaction, and bulimic behaviors, which was about the only thing missing. The main message? EDs don't discriminate.

I was excited to see that my recent survey about sleep/wake habits here on the blog supported my hypothesis: that those with restrictive patterns tend to rise earlier, and those with more binge/purge patterns rise later. Of course, in order to really look at the data, I'd need to compare the early bird and night owl percentages of each category with those of a non-ED sample.

Although many things affect circadian rhythm--most of which are under genetic control--one of the key hormones is cortisol. Released from the adrenal cortex, cortisol levels generally peak upon waking and reach a low point shortly after you go to sleep. What's more, cortisol is released during times of stress or anxiety, increasing both blood pressure and blood sugar.

A PubMed search of eating disorders and circadian rhythm produced mainly results on night eating syndrome. However, one study found a negative correlation between awakening cortisol response and "high anxiety, disinhibition and hunger scores, as well as poor body esteem and a high weight preoccupation" in women, but not men. That means that women with a low awakening cortisol response have high levels of anxiety, poor body esteem, etc. Of course, we don't know if this is cause or effect- just that it exists.

A study in men found a significant relationship between cortisol and perfectionism, which makes sense. Perfectionism is stressful (and don't I know that!), and higher stress means higher cortisol. As well, abnormalities in cortisol have been found in other psychiatric disorders, such as depression.

And indeed, women with anorexia were found not only to have higher cortisol levels but a significant proportion lacked a circadian cortisol rhythm. These abnormal cortisol levels are directly related to the starvation state- after weight restoration, cortisol levels return to normal. I'm not sure how the lack of cortisol rhythm is important. In general, starvation disturbs the sleep cycle, and refeeding is typically associated with improvements in sleep. The general school of thought is that the body is urging the starving person to go get food, and this may be true. But the high levels of cortisol brought out by the stress of malnutrition and starvation may also play a role.

High cortisol levels in people with AN have been positively associated with both osteoporosis and
hyperactivity.

Although one study found that overall daily cortisol rhythms in normal weight bulimic women were pretty much the same as in healthy women, another found evidence of greatly increased cortisol levels. It appears that, in bulimia, cortisol levels might be much higher than usual, although they still have a daily rhythm, unlike in anorexia. Even recovered bulimic patients continued to show a hyperreactivity to corticotropin-releasing hormone, which stimulates the release of cortisol, indicating an underlying neuroendocrine dysfunction.

Yet when cortisol levels were examined in relation to impulsivity, researchers found an inverse relationship between cortisol levels and impulsivity:

Patients with bulimic symptoms had significantly higher rates of cortisol suppression than controls and than restrictive anorectic patients. Percent cortisol suppression showed a strong and significant correlation with the patient's score on the Barratt Impulsiveness Scale. A hypersensitive cortisol response to dexamethasone, which might reflect hypothalamic-pituitary-adrenal axis dysfunctions might be specifically associated with impulsive subtypes of eating disorders.

Clearly, cortisol is just one player on a much larger field. Nor is it clear whether abnormalities in cortisol levels are cause or effect, and perhaps it's a little bit of either. Certainly the eating disorder exaggerates any underlying abnormalities. Whether the ED behaviors themselves cause the specific differences observed in cortisol levels in anorexia and bulimia, or whether these differences are part of the underlying risk factors for these illnesses also remains unclear.

Any questions?