Feasting on Research

The face in the coffee beans

2010-09-15T23:18:00.003-04:00

Howdy everyone. I realize that I've been a little lax at updating this blog- I've been launching my career as a freelance science writer, and that was a giant time suck, to say the least. But now I've gotten established and I'm looking forward to blogging regularly here about the latest ED research. To get you back in the swing of things, I'm starting off with a little brain teaser.

Do you see the face in the coffee beans?

This is one of the neuropsychological tests that researchers have used at the Institute of Psychiatry in London. People with EDs, especially anorexia, are really good at finding the face in the coffee beans. They find it easy to focus on the details and ignore the bigger picture. Essentially, they embody the phrase "can't see the forest for the trees."

These tests aren't diagnostic of anorexia, but they do indicate a detail-orientation, a tendency to lose sight of the big picture (the coffee beans) and focus in on tiny little details that ultimately reveal a face. The "Where's Waldo" books are something similar. For someone with an eating disorder, they will focus on the fact that a Hass avocado has 300 calories rather than focusing on the good fats and oils in the fruit, the buttery taste of guacamole, that California burger they had at a backyard cookout. Or even the need to eat such fats to think better and have shiny, smooth hair. No, an avocado only means 300 calories. Period.

Kara Fitzpatrick at Stanford University gives a talk about the latest eating disorder neuroscience research. It's a series of 3 videos that last slightly over 20 minutes. You can easily just listen to the talk--the visuals aren't utterly crucial.

Part One

Part Two

Part Three

I hope you enjoy!

Bone health and eating disorders

2010-02-16T00:41:00.000-05:00

A recent study from the Journal of Bone and Mineral Research found that women with anorexia had much higher levels of fat in their bone marrow than women without AN (Ecklund et al, 2010). The study was generally publicized as "OMG! Anorexics have FAT on their bony bodies!" Which, as an interesting irony and news hook, I'll give you. But the story goes much deeper than that, which some of the news coverage touched on but really didn't delve into (they appeared to get stuck on the "WTF- could anorexics be fat?!?" part).

Eating disorders are associated with an increased risk for osteoporosis--and it ain't no joke. I've learned that the hard way, with three broken bones and several stress fractures. There are many hypotheses for this increased risk, including deficits in estrogen, high levels of cortisol, and high levels of leptin. I'm guessing each of these plays a role in the decrease in bone mass and density through either the metabolism of bone cells and/or a dramatic decrease in the formation of new bone cells during malnutrition.

This study points to a new mechanism for the dramatic bone density decrease seen in eating disorders in general and anorexia in particular. At the center of larger bones is the bone marrow, one type of which is the red bone marrow and produces new blood cells. The other type is the yellow bone marrow and contains fat cells that can be used as an energy source in cases of extreme starvation. Furthermore, the two types of bone marrow can be interchangeable--in cases of extreme blood loss, the yellow marrow can be converted to red marrow. What Ecklund et al found in this most recent study is that red marrow can be converted to yellow marrow if the body is profoundly starved, which can result in premature osteoporosis.

The study subjects with anorexia had much higher levels of yellow marrow than red marrow, and the researchers hypothesized that the body had prioritized the formation of extra fat for future energy needs at the expense of red blood cell formation (I'm wondering whether this also helps to explain the high levels of anemia seen in people with eating disorders). The innate intelligence of the body never ceases to astound me. In a starving person, fat (which is essentially energy) is much more useful than red blood cells. Without energy, the body shuts off. With fewer red blood cells, you may be more easily fatigued, but mild levels of anemia are rarely out-and-out life threatening.

It will be interesting to see if there is follow-up research done to see how weight restoration and recovery change the ratio of red and yellow marrow, and whether these changes persist for a long period of time after recovery.

Serotonin, antidepressants, and eating disorders

2010-01-23T00:49:00.001-05:00

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.

Of Mice and Men (and Anxiety)

2010-01-20T00:26:00.002-05:00

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.

Hunger may trigger physical activity

2009-12-21T22:32:00.001-05:00

Although a paper from the research journal Nature was typically covered as yet another reason why fat people are fat, it actually has quite a bit of application to eating disorders. The paper, titled "Regulation of adaptive behaviour during fasting by hypothalamic Foxa2," looked at the relationship between hormones released during short periods of fasting and activity levels in mice.

I'll let a press release from Science Daily do some of the explaining for me:

The key switch player in this is a transcription factor called Foxa2. Transcription factors are proteins that make sure other genes are activated and converted into proteins. Foxa2 is found in the liver, where it influences fatburning, but also in two important neuron populations in the hypothalamus -- the region of the brain that controls the daily rhythm, sleep, intake of food and sexual behavior. The control element for Foxa2 activity is insulin, in both the liver and the hypothalamus.

If a person or animal ingests food, the beta cells in the pancreas release insulin, which blocks Foxa2. When fasting, there is a lack of insulin and Foxa2 is active. In the brain, the scientists have discovered, Foxa2 assists the formation of two proteins: MCH and orexin. These two brain messenger substances trigger different behavior patterns: the intake of food and spontaneous movement. If mammals are hungry, they are more alert and physically active. In short, they hunt and look for food. "If you watch a cat or a dog before feeding it, you can see this very clearly," says [lead researcher Markus] Stoffel.

The researchers discovered a disorder in obese mice: in these animals, Foxa2 is permanently active, regardless of whether the animals are fasting or full. This explains a well-known but until now unaccountable phenomenon: the lack of movement in obese people and animals.

To prove this, the researchers used a genetic trick to breed mice, in the brains of which Foxa2 is always active, regardless of whether they have just eaten or are fasting. These mice produce more MCH and orexin and move five times more than normal animals, in which insulin deactivates Foxa2 after eating or which are obese. The genetically modified mice lose fatty tissue and form larger muscles. Their sugar and fat metabolism works flat out and their blood values are considerably improved.

To simplify even further: hungry mice were more active.

Starving people with eating disorders tend to be more active as well. Excessive exercise is very common in people with eating disorders, and is associated with higher levels of anxiety and somatization (that is, physical ailments brought about by psychological stress). Although most people with EDs cite exercise as a way to lose weight or otherwise self-regulate, it may be driven by other biological factors as well.

So why would biology be prodding an organism to get moving when common sense would indicate that they should be resting and conserving every last calorie? One explanation is that a more active animal will move further afield to seek out food. Sitting around won't get you fed; seeking out food just might. Short-term, this is a costly strategy, as there is no guarantee there will be food anywhere else, either. But long-term, you'll definitely starve if you stay in your den where there's no food, so it makes sense.

Of course, for people with eating disorders, the problem isn't the lack of food as much as it is an inability to eat the food that's already there. The body, however, doesn't really care why you're starving. It just knows you are and prods you to go get soemthing to eat, dammit!

The results also help explain how re-feeding, including regular meals and snacks (Stoffel and his snacks-are-bad schtick can go bite me), can help ED sufferers decrease excessive exercise.

There are models of what is termed "activity-based anorexia" in rats, where an animal on a restricted feeding schedule ultimately runs itself to death on an exercise wheel (Epling, Pierce, and Stefan, 1983). Researchers have looked at the role of leptin (Hillebrand et al, 2005) and a-Melanocyte-Stimulating Hormone (Hillebrand et al, 2005b) in activity-based anorexia, with some very interesting and promising results. This latest research only adds to the hormones that may help regulate energy balance in people.

Maudsley Method for Adolescents

2009-12-15T22:20:00.003-05:00

There was a good, basic write-up on the Maudsley Method (aka Family-Based Treatment or FBT) on the blog EmpowHer by a woman who lost her daughter to anorexia nervosa after many years of suffering.

Writes Mary Sornberger:

Dr. Cris Haltom, a licensed psychologist and a Cornell University Ph. D., explains that “The Maudsley Approach is applied to adolescents 18 and under who are living with their families. It is designed to intervene aggressively in the first stages of illness and is a short-term model, as short as twenty sessions or six months in duration.

It is conventional wisdom that recovery is best achieved when eating disorders are treated in the earliest stages, in order to prevent long term, chronic illness.” There is a huge difference in the Maudsley Method compared to other forms of therapy.

The difference is that unlike so many eating disorder therapies, the Maudsley Method does not demonize parents, but after instruction by a trained eating disorder professional, actually puts the parents in charge of re-feeding their own child.

The article is in two parts: Part One and Part Two. These might be a succinct, user-friendly way to explain the treatment you are using for your eating disordered child to friends and loved ones.

Why kids need rules

2009-10-09T17:53:00.002-04:00

This isn't formal research, but I thought it applied to many of you parents who were struggling with how to help your sick children eat. As much as they try to fight you, they also need someone else to impose the consistency of meals and snacks.

A blog post from Psych Central really helps explain how and why kids not only need rules, but they come to like them. Here are a few pertinent quotes:

Kids feel more at ease and secure when they know who’s running the show.

[Kids] know they have a fair chance.

Kids have very few naturally occurring self control skills. Rules, however annoying, make a strong imprint over time inside their little brains. As an adult, they have the skills to start and establish other good habits besides the ones you taught them. It’s the gift that keeps on giving.

ED attitudes in moms of sufferers

2009-09-24T19:11:00.002-04:00

Another reasons for moms to lose their automatic guilt that they "caused" their child's eating disorder: a new study found that the eating disordered attitudes in moms of teens with EDs were the same as those in moms of teens without EDs.

(The full text of the study is in Spanish and can be found here. It's been a long time since high school Spanish, so bilingual folks, please let me know if I've interpreted any of the following totally out of context from the paper...)

The authors hypothesized that mothers of teens with EDs would likely have higher eating disorder cognitions, in part due to the genetic components of eating disorders. And some mothers of ED teens may very well have had higher than usual ED cognitions and behaviors; so might have the mothers of non-ED teens. On average, however, all of the mothers looked the same, even on the different subscales of the Eating Disorders Inventory.

What the authors ultimately concluded was this (with a little help from Google Translate, since they didn't teach some of these verbs in high school Spanish):

"It is interesting to question the myth of the anorexigenic mother who transfers the beliefs and attitudes that get their children sick. A nosological model of cause (the mother) and effect (the eating disorder) does not seem to explain the complexity of this condition."

Reward and punishment in anorexia nervosa

2009-09-07T18:21:00.000-04:00

A recent review article titled "Theoretical perspective on anorexia nervosa: The conﬂict of reward," has to be one of the most fascinating scientific reads I've had for a long time (and my Facebook friends can confirm that I read a lot!). The gist of the paper is that many of the behaviors of AN, such as food restriction and excessive exercise, are initially rewarding, they eventually become punishing. An overlap in the neural circuits that process reward and punishment enables these two factors to become all knotted up, or "contaminated."

The author, Charlotte Keating, begins her argument with the concept of anhedonia, or an inability to experience pleasure, which is central to both major depression and a clinical feature of AN. Moreover, excessive exercisers tend to report greater levels of anhedonia, perhaps because exercise is being misused as a mood elevator. Initially, exercise and food restriction are very rewarding, which may be partly why people with AN become entrenched in these behaviors in the first place. Not eating feels better. Exercising feels better. Continued food restriction and excessive exercise only reinforces the reward, leading to the expectation that not eating and over-exercising will make the person with AN feel better.

The problem, says Keating, is that food restriction and excessive exercise are ultimately rather punishing behaviors. So how can punishing behaviors simultaneously be rewarding? The answer appears to lay in the anterior cingulate cortex, which (among many other things) is involved in the processing of reward, punishment, conflict, empathy, and other rational cognitive behaviors. In people with AN, the ACC doesn't process reward the same way; whether ultimately derived from dopamine circuits, reward is blunted in people with AN.

Writes Keating:

"...it may be that hypoactivity in ACC (which reﬂects the bulk of literature investigating this region in AN) reﬂects an impaired ability to adjust maladaptive behaviors which may also lead to illness maintenance."

Thus reward-punishment contamination means that the AN sufferer has a greatly reduced capacity for motivation to change, and to regulate his/her pathological behaviors. Furthermore, a low motivation for change only increases the neural "blurring" between reward and punishment.

The ultimate goal is not only to improve motivation to change by decreasing the blurring between reward and punishment in AN sufferers, but also to target "the mechanisms that may be responsible for bringing about behavior modiﬁcation."

(cross posted at ED Bites)

Exercise, addiction, and withdrawl

2009-08-17T20:19:00.001-04:00

New research points to the potent addictive effects of excessive exercise. When exercise-addicted rats were given naloxone, a chemical used to block the effect of opiates, they experienced withdrawl effects, such as "trembling, writhing, teeth chattering, and drooping eyelids," whereas inactive mice did not.

From a press release:

The active rats who had access to food for only one hour a day both ran the most and displayed the most severe withdrawal symptoms. Like people with anorexia athletica, they ran so much that they lost significant amounts of weight. Additionally, the more a given rat had run, the worse its withdrawal symptoms after naloxone. In contrast, regardless of how much they ate, inactive rats responded very little to the drug.

Because of the way the active rats responded to naloxone, they seemed to have undergone the same changes in the brain's reward system as rats addicted to drugs. "Exercise, like drugs of abuse, leads to the release of neurotransmitters such as endorphins and dopamine, which are involved with a sense of reward," noted [lead researcher Robin] Kanarek.

Insights into behaviors that trigger the release of the brain's "reward" chemicals may lead to addiction treatments that incorporate moderate exercise, according to the researchers. The findings also suggest that active rats given limited food may make a good experimental model for studying and developing treatments for anorexia athletica, added Kanarek.

The paper itself (free and full-text!), "Running and Addiction: Precipitated Withdrawal in a Rat Model of Activity-Based Anorexia," had some very interesting findings. There, the authors directly linked the commonalities between drug and exercise dependence. They found that "excessive running shares similarities with drug-taking behavior."

Similarities between the effects of exercise and drugs of abuse extend beyond opiate drugs. Research demonstrating that rats will perform operant responses to obtain access to either drugs of abuse or a running wheel provides evidence of the rewarding properties of both drugs of abuse and running. Moreover, under certain circumstances, such as food deprivation, both drug selfadministration and running escalate and become maladaptive behaviors. These findings suggest that running may be able to substitute for drug-taking behavior. In support of this suggestion, rats running in activity wheels self-administered smaller quantities of opiates, alcohol, and psychomotor stimulants (e.g., amphetamine and cocaine) than rats housed in standard cages.

{snip}

The finding that symptoms resembling those of opioid withdrawal occur in food-restricted active rats may have correlates in clinical populations. Excessive exercise is a common symptom of eating disorders, particularly anorexia nervosa Initially, physical activity is used as a means of weight control, but with time it can become an end in itself. In the extreme, individuals with eating disorders can have difficulty refraining from exercise despite adverse physical consequences (e.g., an unhealthy decrease in body weight; decreased bone density; stress fractures). Additionally, symptoms reminiscent of drug withdrawal, including anxiety, depression, and irritability, often develop when these individuals are unable to exercise. The high comorbidity of drug abuse and eating disorders provides further evidence of a common neurobiological basis for these disorders.

The authors also found that female rats showed much higher rates of excessive running than male rats under similar conditions. Furthermore, the authors noted that they were unable to determine whether the withdrawl was specifically due to the increased exercise, or whether it was confounded by differences in food intake and body weight in the active rats.

I would also be curious to see if people with exercise addiction have higher or lower rates of opiate abuse. I could see it go both ways: higher levels of abuse because your system is "primed" for the flood of endorphins, or lower levels because you're getting those endorphins via exercise. It would be interesting to look at how other addictive behaviors overlap in EDs, and whether relatives of those with exercise addiction have higher rates of other addictive behaviors. The authors also suggested that moderate exercise might be a good prescription for those addicted to opiates as it is a non-maladaptive way to get that nice endorphin rush, though I would be hesitant given the known neurochemical overlap between these two addictions.

To me, exercise was a very safe and egosyntonic addiction. Whereas random strangers would have been alarmed if I started shooting heroin (which, given my OCD-related AIDS fears would seriously never ever happen), but they told me how "good" and "dedicated" I was when they learned about just a few of my exercise habits. If exercising X hours each day makes me "good," I figured, then the actual Y hours that I do must make me "fantastic!" I wasn't going to be arrested for having gym shoes on me, or a collection of rank sports bras in my closet. I am almost pathologically risk-averse, so exercise is probably the ultimate addiction for my personality, and I fell in to the trap head-first.

FEAST is on Facebook

2009-08-11T12:13:00.001-04:00

I am super-excited to announce that FEAST is now on Facebook!

Check out the FB FEAST page and feel free to join us (you'll need a Facebook account to join).

FEAST on Facebook

Here, you can keep up on all of the latest FEAST happenings, ask questions, get answers, and otherwise be nosy, Facebook-style.

Please join us!

Great quote!

2009-07-02T22:16:00.002-04:00

I was at a restaurant tonight and I saw this quote over the door:

"All the change that needs to happen in America starts at the dinner table."
--Ronald Reagan

The family as an agent of change

2009-06-26T20:19:00.003-04:00

I found a great article on family-based treatment in Forbes magazine called Teens With Eating Disorders Benefit From Parents' Help. That the title of the article isn't patently obvious to, you know, pretty much everyone is both surprising and sadly expected. However, the exposure of FBT in such places as Forbes online, where it can reach people who might not be specifically looking for information on eating disorders, is pretty fantastic.

A few of the most savory tidbits:

"We know now that eating disorders are real illnesses, not lifestyle choices," Olivio Bermudez said. And parents can play a crucial role in recovery, Bermudez and others now believe. In fact, researchers found that teens were more able to control their disordered eating when they had family support.

"The therapist works with the family to empower the family to get the [anorectic] child to eat the meals and recover the weight," Bermudez said. "The family becomes the agent of change."

The article ends with a series of "suggestions" for parents, although one of them left me cringing a little bit, as parents are instructed to "follow the directions" of the treatment team. I would have love to have seen this rephrased as "parents are part of the treatment team," and that they should certainly listen to the treatment professionals, but all clinicians are not created equal.

Still, it's a solid article about FBT.

In the next day or so, I have a few more research-oriented articles for you, so hold onto your seats.

F.E.A.S.T. in Time Magazine!

2009-06-25T13:07:00.002-04:00

F.E.A.S.T. made an appearance in a Time Magazine piece this week: A Genetic Link Between Anorexia and Autism?

High cholesterol in anorexia nervosa

2009-05-24T12:57:00.001-04:00

One of the (many) paradoxes of anorexia is that the excessive weight loss that accompanies the disorder often results in high cholesterol levels. This seems to go against what many doctors and researchers say about cholesterol: decreasing food and fat intake as well as increasing exercise should decrease cholesterol levels, not raise them.

It turns out that this high cholesterol (formally known as hypercholesterolemia) also happens to starving people, and is a well-known side effect of malnutrition. The question that remains, then, is why? Why this paradoxical effect?

Let me back up a bit and explain what cholesterol is and what it does. Cholesterol "is a lipidic, waxy alcohol found in the cell membranes and transported in the blood plasma of all animals. It is an essential component of mammalian cell membranes where it is required to establish proper membrane permeability and fluidity." Cholesterol is hydrophobic, meaning it doesn't dissolve in water or blood, so it is transported in the body by lipoproteins. Your total cholesterol count is a combination of triglycerides, low-density lipoproteins (LDLs, aka "bad" cholesterol) and high-density lipoproteins (HDLs, aka "good" cholesterol). Both LDLs and HDLs transport fats along with cholesterol. The lipid hypothesis holds that there is a causal link between high intake of saturated fats, hypercholesterolemia, and heart disease, promulgated by none other than Ancel Keys, he of the Minnesota Starvation Study.

So. What does this all mean?

Besides just having unusually high levels of total cholesterol, patients with anorexia were found to have unusually high levels of an enzyme called cholesterylester transfer protein (CETP), which swaps cholesterol and fat molecules between the different lipoproteins. The researchers speculated that low levels of thyroid hormones and low breakdown of existing cholesterol contributed to high cholesterol levels, and that "CETP activity increases cholesterol turnover as an adaptation to its low intake." The highest levels were seen amongst AN patients who also binged and purged. In severely malnourished AN patients, however, cholesterol levels and CETP activities drop dramatically.

Other studies have suggested that starvation results in the increased synthesis of lipoproteins. It could also be that these lipoproteins are transporting fats in the body, which the body is relying on as fuel due to insufficient food intake. If the body is going to rely on fat as fuel, it needs some way to mobilize those fat molecules and get them to a location where they can be broken down effectively. This could perhaps explain the abnormal rise in cholesterol levels. As body fat is essentially depleted in the severely malnourished AN patients, the body may rely more and more on breaking down organ and muscle tissue, thus decreasing the need for abundant lipoproteins.

Regardless of the reasons for hypercholesterolemia during anorexia, it is NOT an indication that the sufferer needs a low-fat or low-cholesterol diet. With sufficient foot (and fat!) intake, cholesterol levels typically right themselves rather rapidly.

(cross-posted at ED Bites)

Self-harm and glucose metabolism in women with EDs

2009-05-19T00:04:00.001-04:00

Self-injury (such as cutting or burning oneself) is fairly common amongst people with eating disorders- approximately 25% to 45% of people with eating disorders self-injure, and approximately half of those who self-injure also have eating disorders (full article here). Many people report a sense of dissociation while self-harming, a desire to turn emotional pain into physical pain (ie, "real" pain), and also that this behavior reduces anxiety. Whether self-harm is from issues relating to impulse control, a more compulsive pattern of behavior, or something else entirely, the amount of overlap between self-injury and eating disorders is significant.

An interesting new paper from the journal Psychoneuroendocrinology looked at the relationship between self-injury and glucose metabolism in women with eating disorders, and what they found was significant. Women engaging in self-harm behaviors were given an oral glucose tolerance test, in which they were asked to drink a sweet solution to measure how the body handles sugar. The self-harming women who also had an eating disorder had higher levels of blood glucose after the test, but also higher levels of a hormone called glucagon.

Glucagon is essentially insulin's opposite: when the blood sugar is low, the pancreas secretes glucagon to prod cells into breaking down long chains of carbohydrates called glycogen into small sugars that can be released into the bloodstream and readily used by the body. When blood sugar rises after a meal, the pancreas secretes insulin, which stimulates cells to pull excess sugars out of the bloodstream and store them as glycogen for a rainy day*.

Besides low blood sugar, several other factors can stimulate the release of glucagon, including epinephrine (aka adrenaline), which is involved in the fight or flight response. Though I was unable to find any specific studies linking high levels of epinephrine and self-injury, it's certainly plausible to think that people who self-harm would have higher levels of epinephrine, especially right after an incident where such behavior occurs. Alternately, if high levels of glucagon also stem from high levels of epinephrine, the sufferer may be caught in a cycle of self-harm during episodes of low blood sugar.

For instance, a common pattern in those who binge and purge is binge-purge-self harm, where the self-harm typically occurs after the completion of the binge/purge cycle. After a binge, blood sugar goes up and glucagon levels go down. After a purge, blood sugar goes down, and glucagon and epinephrine levels go up.

No one knows at this point where the relationship between self-harm and glucose metabolism lies on the cause/effect scale. Certainly there is a feedback cycle between all of these systems. But one good point to keep in mind is the importance of helping sufferers regulate blood sugar levels by frequent meals and snacks that involve complex carbohydrates, proteins, AND fats. Food is medicine for the eating disorder, but it also might be true for self-injury.

*Aren't you glad I paid attention in my 8am biochem lecture 10 years ago?

(cross-posted at ED Bites)

Psychiatric Advance Directives: A Tool for Adult Sufferers

2009-04-13T00:12:00.004-04:00

Several questions arose on the Around the Dinner Table forum about what to do when a child turns 18. In the US, 18 means a person is in charge of his or her own medical decisions, and parents have to ask permission to view medical records and are not implicitly part of the decision-making process when it comes from determining proper care for their child's eating disorder.

So what should parents do before their eating disordered child turns 18?

My answer to this question depends a little bit on their status in recovery. If your child is still acutely ill, getting them to approve a psychiatric advance directive may be difficult. The eating disorder will probably not like this idea very much. However, if they are thinking more rationally and are embracing recovery at least somewhat, this may be an opportunity to prepare one of these documents.

What is a psychiatric advance directive, anyway?

They're a lot like a living will, except for psychiatric care. The idea of the document comes from the understanding that mental illness frequently robs the sufferer of the ability to make the best decisions for their own care, especially when the illness becomes severe. Mental illness can also rob a person of the ability to even understand that they are ill, which can lead to court-ordered treatment. Although this treatment is certainly life-saving, it also prevents a sufferer and his/her family from having much say in the course of treatment.

A psychiatric advance directive is typically written during periods of recovery/remission, and spells out the kind of care the sufferer would like to receive if their illness ever renders them incapable of making these decisions in the future. Furthermore, the sufferer can specify an "agent" (such as a parent/guardian/caregiver) to make these decisions in their place.

The sufferer can provide instructions on hospitalization, alternatives to hospitalization, medications, treatment, etc. The document can specify who should be contacted if the individual does end up in a psychiatric unit, who should take temporary custody of any children, etc. The document must be signed by the sufferer, two witnesses and then notarized.

The Bazelon Center for Mental Health Law says that psychiatric advance directives have three main advantages:

An advance directive empowers you to make your treatment preferences known.
An advance directive will improve communication between you and your physician. It can prevent clashes with professionals over treatment and may prevent forced treatment.
Having an advance directive may shorten your hospital stay.

Laws vary from state to state, and psychiatric advance directives have not been tested much at all in courts of law. However, it may be a useful tool in helping to protect an adult child in the event of a future relapse.

More information on psychiatric advance directives:

From The Bazelon Center for Mental Health Law
From The National Alliance on Mental Illness
From Duke University
FAQs on psychiatric advance directives
National Resource Center on Psychiatric Advance Directives
Templates for creating an advance directive

If you have any questions, I would consult with a family lawyer. They would be able to answer most questions you might have.

Nice write-up on Maudsley Method

2009-04-02T15:39:00.002-04:00

A really basic summary at Health News Digest provides a quick, easy read explaining the Maudsley Method (in other words, it's a good handout for people involved in your child's life who need to know the what/why/how of your treatment approach). The story, titled "Milkshakes Are Medicine for Anorexic Teens in Family-Based Outpatient Therapy," looks at research going on at New York's Weill Cornell Medical Colleage comparing family-based treatment to traditional psychotherapy.

Two winning quotes:

"In Maudsley, food is medicine that restores the body and mind. When the body is starving, the mind also weakens, becoming more susceptible to anorexia's rigid, often obsessive logic. Supervised feeding helps to break this vicious cycle. With the anorexia in charge, the adolescent really cannot regain the weight on his or her own. Nutritional rehabilitation gives the brain the nutrition it needs to re-establish healthy eating habits," says Dr. Dara Bellace, a clinical psychologist at NewYork-Presbyterian Hospital/Westchester Division and an instructor of psychology in psychiatry at Weill Cornell Medical College.

"This approach does not blame parents, but rather calls on their ability to nurse their child back to health. It requires a strong commitment to be with them for every meal -- something that can mean rearranging schedules and taking a tag-team approach to sharing the responsibility," adds Dr. Bellace. "The adolescent must also dedicate themselves to the therapy, understanding that, until they regain the weight, their parents will be feeding them much as they did when they were younger, deciding what and how much they eat and making sure they finish."

Happy reading!

The last five pounds matter

2009-04-01T23:16:00.003-04:00

Determining a healthy body weight for someone suffering from an eating disorder, especially if they are not yet done growing, seems as much art as it is science. (More information on how to determine ideal body weight can be found here) Yet the importance of setting a high-enough weight is rarely discussed, especially in an environment full of fears of childhood obesity.

It turns out that settling for a body weight even slightly below an individual's healthy set point can have long-term effects. A group of researchers at Schneider Children's Hospital examined the relationship between body weight, metabolism, and menstrual status in a group of normal weight adolescents with a history of AN, BN, and/or EDNOS. In a subset of these patients, resting energy expenditure was measured via indirect calorimetry.

The non-menstruating adolescents had an average of 98.5% ideal body weight, while adolescents with regular menses had 102.8% ideal body weight. Furthermore, the amenorrheic group had a significantly lower resting energy expenditure, indicating that their bodies were still operating as if their diets were restricted. In fact, this group also consumed a lower-fat diet than the menstruating group, which tacitly implies that these teens were still restricting their diets, even if their weight was within the "normal range."

In growing teens, even a short duration of amenorrhea can result in significant bone loss which can only be restored by full weight restoration and the resumption of menses.

Although the authors state that, "It is unclear whether participants with amenorrhea, despite achieving a BMI percentile of 47.6%, would require an additional, yet modest, amount of weight gain to resume menses," the dangers of not requesting that recovering ED patients gain a few more pounds seems to far outweigh any temporary discomfort of the adolescent.

"Perhaps metabolic recovery alone, where the focus would be to correct the caloric imbalance and increase dietary fat, would be sufficient. In addition, it would be helpful to determine the impact of a participant’s premorbid weight on influencing the chances for resumption of menses," the authors conclude.

(On a personal note, that ED specialists are trying to determine IBW without taking premorbid weight into account is quite disturbing, though not really all that surprising)

The weight differences between the two groups of adolescents was not that significant- approximately five pounds. Yet their nutritional statuses showed very different pictures. Although other factors certainly do play a role in the resumption of menses after an eating disorder, even slightly lower weights can make a huge difference both short- and long-term.

Which came first...

2009-03-24T21:52:00.000-04:00

...the over-protective mother or the anxious child?

According to a new study from the Journal of Clinical Child & Adolescent Psychology, over-protective mothering appears to be a "natural response" to anxious children.

The researchers, led by Jennifer Hudson of Macquarie University, knew from previous researchers that the mothers of anxious children tended to be over-protective and over-involved. What they didn't know, said Hudson, was "whether it is the child's anxiety that brings out over protective behavior."

For this study, titled "Child and Maternal Influence on Parenting Behavior in Clinically Anxious Children," the researchers compared clinically anxious children to their non-anxious counterparts as they interacted with mothers not their own. Hudson's group found that "when mothers interacted with an anxious child, they provided significantly more help to the child than mothers interacting with a child who did not have an anxiety disorder. "

"These results suggest that over-protection is a normal response to an anxious child and not the fault of the mother," Hudson said. "These findings may help reduce parental feelings of guilt and blame and may help parents understand their own and their child's behavior."

Many mothers of eating disordered children are accused of being over-protective, and many eating disordered children also show pre-morbid anxiety traits or disorders. This indicates that mothers of ED'd children may perhaps be more over-protective but that this is not necessarily indicative of any pathology on the mother's behalf. It's just a natural response to an anxious child.

Hypermetabolism: the basics

2009-03-19T22:39:00.003-04:00

Many people recovering from AN experience hypermetabolism, a common phenomenon that is often overlooked. I did some more research tonight into the biology and etiology of hypermetabolism. So let's start with a basic definition from Wikipedia:

Hypermetabolism is the physiological state of increased rate of metabolic activity. The impact of the hypermetabolic state on patient nutritional requirements is often understated or overlooked. Hypermetabolism typically occurs after significant insult to the body. In hospitals and institutions, the most common causes are infections, sepsis, burns, multiple trauma, fever, long-bone fractures, hyperthyroidism, prolonged steroid therapy, surgery and bone marrow transplants.

And, yes, eating disorders. Specifically anorexia. As someone falls deeper and deeper into anorexia, their metabolic rate slows dramatically. During the Minnesota Starvation Study, resting energy expenditure (also known as basal metabolic rate- the amount of calories needed just to keep your body functioning and doesn't include ANY physical activity) fell by about one-third. The book "Introduction to Clinical Nutrition" says that

Starvation involves metabolic alterations that enhance the chance of survival by increasing the use of body fat stores, by sparing the use of glucose, by minimizing nitrogen loss, and by decreasing energy expenditure.

But when the ill person begins eating again, their metabolism kicks into high gear. Body temperature rises. A person can experience night sweats, which may also be related to hormone function returning to normal. Why? It seems a remarkably inefficient use of resources. And indeed, hypermetabolism may not be entirely adaptive from an evolutionary standpoint as the body's use of food becomes remarkably inefficient. Even so, the body needs tremendous amounts of energy to replace lost fat and muscles stores, depleted organs, bone mass, hair, nails, you name it. No organ system is spared during an eating disorder.

The amount of calories needed for people with anorexia to return to a healthy weight can vary by illness severity (a lower BMI means more calories, as well as duration of illness), and by illness subtype. One study found that those with the binge-purge subtype of anorexia needed significantly fewer calories than those with the restricting subtype; another study found that calories were about the same. Other variants include your metabolic rate before illness onset. I've known several good friends curse their fast metabolisms quire vociferously during refeeing.

When looking at the phase after weight restoration, caloric needs between people with anorexia nervosa and those with bulimia nervosa turn out to be quite different. One study found that people with AN needed more calories per kilogram of body weight than normal controls, while those with BN needed fewer. It appears that people with a current diagnoses of BN but a history of AN require more calories than those with BN alone. Further, people with the restricting type of AN needed more calories than those with the binge-purge type, both of which were greater than patients with BN (some of the studies cited above show that, for weight maintenance, caloric needs are basically the same for any patient with a current diagnosis of AN).

Some of these differences may rest in premorbid differences in metabolic rate. It makes intuitive sense that a person who finds it easy to lose weight would have a faster innate metabolism. Other reasons calorie needs may remain unusually high for a person even after weight restoration is the sheer amount of rebuilding the body needs to perform. Bulimia is violently destructive to the body, and I would never say differently. However, some of the damage done by anorexia is slightly different, and the body must rebuild and repair essentially every organ in the body. My psychiatrist told me that the nerves continue to repair themselves for up to two years after weight restoration. This can hardly be the only organ system taking a long time to recover.

How long hypermetabolism lasts will probably vary from person to person, and depends on how long you were sick, how your body responded to the damage from your eating disorder, your activity levels, among others. There's no real way to be sure. If your caloric needs are unusually high--even for hypermetabolism--you can have body composition analysis and resting energy expenditure testing done. Personally, I think this is best left to extreme cases since so many sufferers have a tendency to fixate on numbers.

I hope this helps explain hypermetabolism just a little bit. I can't answer every question, as it's been a long time since my college biochemistry days, but I can always look things up.

Cortisol and eating disorders

2009-03-19T22:31:00.002-04:00

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.

In otherwise healthy women who did not have regular menstrual periods, cortisol levels were increased compared to normal women, indicating stress on the body (the authors hypothesized that the reason for this amenorrhea was insufficient fat intake, despite sufficient calories and without excessive physical activity).

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 andhyperactivity.

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.

(originally posted at ED Bites)

Long time, no write

2009-03-19T22:23:00.002-04:00

Hi everyone.

My apologies for not writing recently- I had just started a new job in Washington, DC and was trying to move and get all my stuff organized. As well, I did some freelance writing that culminated in a Washington Post article on the Maudsley Method titled "A girl's suffering drove her parents to try a new anorexia treatment."

I do have several topics in the pipeline. However, there are one or two posts from my other blog ED Bites that might be of interest to parents, so I'm reposting them here. The first one is on hypermetabolism. The second is on cortisol and EDs.

Happy reading everyone!

Hostility during refeeding

2008-10-26T22:04:00.004-04:00

Admittedly, this isn't research. It's an observation by author and anthropologist Sharman Apt Russell in her book Hunger: An Unnatural History. Although only a chapter is spent looking at anorexia nervosa in particular, the book is haunting and well worth a read.

Russell spends much time on events that took place during World War II: the Minnesota Starvation study, the Dutch Hunger Winter, and the tragedies in the Warsaw Ghetto. This excerpt is from Russell's summaries of the refeeding portion of the Starvation Study- the most important part. After all, the purpose of the study was not just to learn what exactly happened when people starved (that was generally well known). It was also to learn how to most effectively refeed a group of starving people on the lowest amounts of calories, funded by the war effort to help keep Europe out of Communist hands after the Nazis surrendered.*

But the men were not initially allowed free access to food. Their calories were only increased slowly, much to the chagrin of the men who thought that their ordeal would finally be over. They got irritable, cranky, desperate.

From Russell:

By the end of the sixth week of refeeding, almost all the subjects were in active rebellion. Many "grew argumentative and negativistic." Some questioned the value of the project, as well as the motives and competence of the researchers. A few admitted that their desire to help the relief effort had completely disappeared. At the same time, unnoticed by the subjects themselves, their energy was returning. They became more responsive, albeit in a negativistic way. They were annoyed at the restrictions still imposed on them. They rejected the buddy system, which was removed "in the face of imminent wholesale violation." They resisted going back to a regular work schedule. At times, the experimenters felt they were watching "an overheated boiler, the capacity of the safety values an unknown variable."

Later, the researchers compared this with what they learned about refeeding camps after the war, where aid workers also noted a growing aggressiveness and surprising "lack of gratitude" in men and women who had previously been dull and apathetic with hunger.

So it seems from these anecdotal cases that some of the resistance seen by eating disordered children during refeeding seems almost purely organic and NOT related to the eating disorder. Perhaps the brain is reawakening and is not happy. Perhaps the person is unable to process what the hell just happened. The anxiety around food that is, of course, related to the eating disorder, seems only to make this worse.

But the negativity and hostility may also be the intrinsic response of a starving brain.

*I thought this was fascinating- obviously, because I included it.

FBT for bulimia in single-parent families

2008-10-12T20:16:00.003-04:00

Despite its efficacy in studies, family-based treatment isn't for every family. For single-parent families, FBT can be "ruled out" as a treatment approach because of the time-intensive nature of treatment. Every meal, every snack, every day.

Of course, single-parent families can make it work. The other parent may be nearby and willing to help. Other caring adults can pitch in, or other family members. The parent may be able to take time off of work to care for their sick child until s/he is able to manage better on their own.

But the efficacy of FBT in single- vs. double-parent families hadn't been studied. In the International Journal of Eating Disorders, Daniel LeGrange and the team at the University of Chicago found that single-parent families were able to help their teens with bulimia nervosa as effectively as double-parent families.

Writes LeGrange in the introduction of the paper:

Given the emphasis in FBT on the involvement of the entire family in helping to reduce binge eating and purging behaviors, it could be that single-parent families demonstrate poorer outcomes than two-parent families receiving FBT. Although there is no research indicating that individuals from single-parent families have poorer outcomes in FBT for BN, there are several lines of indirect evidence to suggest that family status may relate to treatment outcomes.

First, single parent families may have less time, fewer social supports, or fewer financial resources than two-parent families. This could predispose single parents toward premature autonomy-granting or decrease their ability to provide adequate parental monitoring.

He also cites unconscious therapist bias against single parents being able to make FBT work, as well as evidence from AN treatment. Single-parent families battling AN benefit from 12 month FBT as opposed to the shorter-course 6 month treatment.

However, LeGrange et al. found:

There were no statistically significant differences between two-parent and single-parent groups on any of the treatment variables at post-treatment or 6-month follow-up...Patients in both groups showed significant reductions in eating disorder behavior and depressive symptoms as well as increases in self-esteem.

Part of the reason that FBT is just as effective in single-parent families is that in dual-parent families, responsibility isn't always shared equally between parents.

The study concluded:

Despite the reliance on parental intervention to reduce bulimic symptoms and normalize eating patterns, the results of this study suggest that FBT is an appropriate and efficacious treatment for single-parent families as well as two-parent families.

Predicting Anxiety Disorders

2008-09-17T20:33:00.002-04:00

Anxiety disorders are some of the most common brain diseases amongst adults and teens. Walter Kaye found that an anxiety disorder is the strongest risk factor for an eating disorder. That researchers have found a better way to predict anxiety in teens is important in and of itself, but it might also be able to identify people at a much higher risk for eating disorders.

Says a summary of the research on Science Daily:

Craske and her colleagues are finding that neuroticism — the tendency to experience negative emotions such as fear, anxiety, guilt, shame, sadness or anger — is a powerful predictor of both anxiety and depression. Newly published research from the long-term study highlights a potential mechanism by which neuroticism confers risk. The researchers report that teenagers who are high in neuroticism appear to become unnecessarily anxious in ways that are out of proportion with actual circumstances.

Neuroticism is also a common trait of people with eating disorders, especially those with anorexia nervosa.

Furthermore:

"This is interpreted as neuroticism leading to enhanced anxiety under conditions associated with aversive events but in which negative events themselves are very unlikely," Craske said. "It may represent a failure to distinguish conditions that are safe from conditions in which threatening events are very likely to occur. By translation, these findings suggest that persons with high neuroticism would respond with appropriate fear to actual threatening events, but with additional unnecessary anxiety to surrounding conditions. This type of responding may explain why neuroticism contributes to the development of pervasive anxiety."

Craske and her colleagues report their findings this month in the journal Biological Psychiatry. She hopes the study will reveal the risk factors that predict anxiety, versus depression, and which risk factors are common to both anxiety and depression.

"Anxiety and depression often go hand in hand; we're trying to learn what factors place adolescents at risk for the development of anxiety and depression, what is common between anxiety and depression, and what is unique to each," Craske said.

It would be interesting to see whether this leads to any better predictions of what traits in what people predispose them to eating disorders.

Because many eating disorder prevention efforts are targeted more generally at improving self-esteem and media literacy, and important population at higher risk may be overlooked. Perhaps these teens would benefit from lessons in decreasing perfectionism and increasing resilience. No doubt it would help with anxiety. Might it also help with eating disorders?

Eating Disorders and Athletic Participation

2008-08-23T22:56:00.002-04:00

With the passage of Title IX, more and more women have been participating in athletics. Although participation in sports has many benefits--including teamwork, fitness, and fun--it also brings a risk of eating disorders, especially at an elite level. A recent study from the International Journal of Eating Disorders, led by Jill Holm-Denoma (now of the University of Denver), looked at eating disordered attitudes and behaviors in relation to level of athletic participation and sports anxiety.

Women who participate in intercollegiate varsity athletics have much higher rates of eating disorder symptomatology when compared to women in club sports, independent exercisers and non-exercisers. Furthermore, higher levels of sports anxiety (that is, anxiety about physical activity and/or sports) were predictive of increased levels of bulimic symptoms and a drive for thinness.

Varsity athletes have devoted much of their recent lives to their sport, increasing both their identity with athletics and the pressure to perform well. As well, it could be that eating disordered attitudes and behaviors are normalized, tolerated, or even encouraged. Traits of obsessionality and perfectionism are risk factors for eating disorders, that may also cause a woman to excel at the varsity level.

Yet the results show an interesting variation. Writes Holm-Denoma:

Despite the trend for women who participated in higher levels of athletic competition to have higher levels of eating disorders, our data do not suggest a clear dimension ranging from nonexercisers to varsity athletes. In some cases, for instance, independent exercisers appear to have similar traits to varsity athletes (e.g., see Fig. 1). Thus, some independent exercisers may engage in exercise as frequently and/or intensely as women who participate in competitive athletics.

It appears that some women with eating disorders (or their accompanying attitudes) exercise alone, independently, and perhaps obsessively. This could perhaps come from a desire to hide their disorder.

The researchers conclude that:

Coaches and clinicians should be aware that athletes experience higher rates of eating disorder symptoms than nonathletes. Moreover, sports anxiety should be considered as a possible target of therapy among athletes.

(cross-posted at ED Bites)

Sobering Statistics

2008-08-21T21:20:00.003-04:00

A recent story from the News Observer had these startling statistics to remind everyone why early treatment of eating disorders is essential:

20 percent of adults overcome their eating disorder, compared with an 80 percent recovery rate among adolescents.

Given that most eating disorders start in adolescence (most estimates range from 13-18 as the peak years of onset, with bulimia generally beginning at a later age than anorexia), most adults have been suffering for years, if not decades. The disease at this point has become entrenched, a part of the sufferer's life.

There are also no researched, effective treatments for adults, in part due to the chronicity, as well as the difficulties in compelling a loved one into treatment for long enough to reach a stable, healthy weight.

In the book "Hunger: An Unnatural History," a famine relief worker said that malnutrition in children is always easier to treat than in adults. Part of it is, he says, the greater resilience of young bodies. But the other part is the simple power of a mother urging her child to eat.

Other statistics from the story:

80 percent of eating disorders start out as diets.
Ten million women in the U.S. have an eating disorder, according to the National Eating Disorders Association.
79 percent of deaths from anorexia occur in people who are over the age of 45.

Administrative Update

2008-08-17T23:02:00.002-04:00

Sorry for the lack of posts lately- I'm trying to find a place to live and apply for jobs, so I have been both busy and stressed.

At any rate, I just posted a huge list of links of free full-text research articles on the right-hand side of the page. Please email me any other articles you might have that you think will be of use to parents at carrie [at] edbites [dot] com and I will post them as soon as I am able.

Lastly, I found that the parent book that accompanies "Next to Nothing" is now available for free download online:

If your adolescent has an eating disorder

You will need Adobe Acrobat to read the book (and no, I didn't write a single word of it!).

I'm hoping to have one or two things up this week, depending on how quickly I can pack up my apartment.

Starving in the Midst of Plenty

2008-07-31T23:23:00.004-04:00

One of the characteristics of anorexia, says researcher and clinician Daniel LeGrange, is not just starvation; rather, he says, it is starvation in the midst of plenty. While one theory is that anorexia may have evolved as an adaptation to allow humans to better withstand famine, most modern cases of anorexia occur where food is abundant. In that sense, perhaps anorexia can be understood as self-administered starvation.

Which is where a recent study on cocaine addiction comes in.

A recent study from the University of California, San Francisco found that self-administered cocaine had different effects on dopamine receptors than a passive infusion of the drug.

Says a press release:

...cocaine-associated changes were due to an associative process and not just to the pharmacological effects of the drug. "We suggest that neuroadaptations induced specifically by drug self-administration may form a powerful 'memory' that can be activated by drug-associated cues," explains coauthor Dr. Billy T. Chen.

How self-administration of a drug but not a natural reward can elicit enduring changes within the brain remains a mystery. "Future studies are required to identify the exact mechanisms through which drugs of abuse alter neural circuitry that is normally accessed by naturally reinforcing events but is usurped by cocaine to persistently cement these synaptic adaptations, perhaps ultimately leading to pathological drug-seeking behavior," concludes Dr. Bonci.

While anorexia is not cocaine addiction, the illness does involve differences in dopamine levels and receptors in the brain. Perhaps part of what cements anorexia (besides the starvation itself) is the self-seeking behavior. The "benefits" of starvation to the sufferer are reinforced each time he or she skips a meal, binges, purges, and overexercises.

From an evolutionary standpoint, the survival of the human species means that people will need to begin eating after a famine has passed. The ability to withstand starvation may have descended from this. But anorexia nervosa may cement itself into a life-threatening illness when a person begins to starve while food is abundant.

FBT: Two case studies

2008-07-27T21:28:00.002-04:00

I found two case studies of success with Family-Based Treatment (Maudsley) that was published in the Mayo Clinic research journal.

You can read the pdf here: Family Based Therapy for Adolescents with Anorexia Nervosa

On a personal note, what I found especially illustrative were the charts of the weights of the teens (one girl, one boy) on pages 3 and 4.

I intend to compile some of these links and post them in the right-hand column. I'll be working on this, and a longer article on dopamine, over the next week.

Self-reported eating disorder symptoms differ between adolescents and parents

2008-07-27T17:50:00.002-04:00

Part of the difficulties in diagnosing an eating disorder is finding out precisely what's going on, both behaviorally and psychologically. Traditionally, professionals have relied on patients to self-report thoughts and behaviors. Given the secretive nature of eating disorders, this certainly makes sense. There may be other things going on that the sufferer is hiding from friends and family. And a sufferer may not always vocalize their thoughts and feelings to loved ones, perhaps feeling threatened or vulnerable, or not wanting people to worry.

Yet eating disorders--especially anorexia--are anosognostic. That is, the very illness the person has prevents him or her from seeing that they are ill. It's subtly different than denial. When a person is said to be "in denial," which is common with substance abuse and other addictions, he or she inherently knows that something is wrong, but it unwilling or unable to admit it. With anosognisia, the person literally doesn't understand that there is a problem. I wanted to lose weight, and I did, thinks a sufferer. What's the problem?

Which makes the self-reporting of symptoms, behaviors, and thoughts inherently problematic. Researchers in Germany recently compared surveys and forms comparing reports of physical and psychological issues confronted by ED patients. It turns out that parents consistently rated their children as having more severe thoughts and behaviors than their adolescent.

The researchers conclude:

Agreement between parents and adolescents regarding the presence and severity of psychiatric symptoms in adolescents with ED is low. In contrast to previous studies in non-ED samples, adolescents with ED reported lower levels of internalizing problems than their parents. Denial and minimization may be underlying reasons for our findings and represent obstacles in the psychological assessment of adolescents with ED.

Therefore, it is crucial to make sure parents are included not only in treatment, but also in the diagnosis of their child's eating disorder.

Unearthing anorexia's genetic roots

2008-07-09T22:20:00.003-04:00

While eating disorders remain complex, multifaceted brain diseases, research is uncovering the importance of genetics in causing these diseases. Some families have long known that eating disorders, like other illnesses such as depression, bipolar disorder, and anxiety disorders, run in families.

The question that has remained is how: how are risks for these illnesses inherited? And what are these risks, anyway? Despite all of the talk, there will almost certainly be no "anorexia gene" or "bulimia gene" uncovered. Issues likely involve differences in appetite regulation (especially the hormones leptin and ghrelin), and altered levels of the neurotransmitters serotonin and dopamine, which regulate mood.

Abnormal levels of serotonin have also been found in those with obsessive-compulsive disorder, an anxiety disorder that is several times more common in those with anorexia nervosa.* The close links between OCD and AN have prompted some researchers and clinicians to question whether anorexia should be classified as an obsessive-compulsive spectrum disorder. This spectrum includes Tourette's syndrome, tic disorders, compulsive skin picking, trichotillomania (compulsive hair pulling), and body dysmorphic disorder. All of which are, not surprisingly, more common in people with anorexia than in the general population.** This confirms and strengthens the contribution of serotonin to anorexia.

Now, researchers have made links between anorexia and what appears to be the illness' mirror image: 'bigorexia,' or muscle dysmorphia. Those who suffer from muscle dysmorphia, almost exclusively men, believe themselves to be small and unfit. Their response (again, the eerie mirror image of anorexia) is to bulk up through weight lifting, special diets, and occasionally injectible steroids.

The initial commonality between anorexia and bigorexia are the obvious body image distortions. But the similarities may go deeper than that. Finnish researchers studied five pairs of twins, which included at least one male with anorexia nervosa in each twin pair. A story on Reuter's Health revealed that the researchers found "a 'striking familial liability' for traits related to the eating disorder, including major depression, muscle dysmorphic disorder (which is sometimes called 'bigorexia), and obsessive compulsive disorder. The findings suggest that all of the symptoms have similar genetic roots, the researchers point out."

Just as telling, eight out of the ten twins had suffered from a mood disorder during their lifetime. And body dysmorphic disorder (especially muscle dysmophia) was common in the twins without AN.

The abstract of the study says this: In males, overweight commonly predated AN, and symptoms of body dysmorphic disorder, particularly of muscle dysmorphia, were common among the anorexia-discordant co-twins. Affective and anxiety disorders were present in both the probands and their co-twins. CONCLUSION: We found a strong familial clustering of AN, affective and anxiety disorders, and symptoms of muscle dysmorphia among men in the general population. In men, muscle dysmorphia may represent an alternative phenotype of AN.

While a study involving five pairs of twins is by no means conclusive, the link to muscle dysmorphia and mood disorders implicates a serotonin dysfunction as a contributing factor to anorexia and the body image disturbances that so often accompany it.

*And the reverse is also true: those with OCD are more likely to have AN or BN. Although this study out of Spain provides evidence that eating disorders and OCD might not be related.
**Sadly, research on bulimia, EDNOS, and binge eating disorder is limited at best.

(Cross-posted on ED Bites)

Family Based Treatment is Cost-Effective for Adolescent AN

2008-07-01T23:01:00.000-04:00

There's no way around it: anorexia (and other eating disorders) are difficult, expensive illnesses to treat. The good news is that effective treatments are available. Recovery can be a long, winding road (as I and other families know), but new research is showing the most effective ways to treat anorexia.

James Lock and his group out of Stanford University published an article in the latest issue of Eating Disorders: The Journal of Treatment and Prevention, titled "Costs of Remission and Recovery Using Family Therapy for Adolescent Anorexia Nervosa: A Descriptive Report." He looked at the costs to treat adolescents with AN and their families with a standard Family-Based Treatment approach.

The majority of the costs (72%), Lock found, were due to medical hospitalization, before or during outpatient treatment. Another 20% were due to outpatient psychiatric treatment, a much smaller percentage than is traditionally given. Noted Lock: "This result may be due to the specific outpatient management strategy used in this study which employed parents as the main agents for change. In cases where this approach is effective, this results in decreasing both the intensity of treatment as well as the need for other types of treatment such as individual, group, nutritional counselling, or other forms of treatment that would add expense."

Due to differences in insurance, the final costs listed in the paper did not factor in health coverage, or any deductibles and co-pays. The costs listed, then are the market cost of treatment and NOT what most people with insurance coverage would pay. Costs, however, would still be extensive. The study also failed to factor in food costs (which can be significant) and extraneous costs such as time off work for parents. Obviously, this would vary greatly from family to family, but again, these costs are significant.

Lock found that costs to recovery can vary widely, ranging from USD$33,000 for "partial remission," defined as weight >85% IBW, to USD$84,000 for full recovery (weight >95% IBW and Eating Disorder Examination scores in the normal range). This treatment is more expensive than that of even schizophrenia. But, considering that the average residential treatment stay lasts for 90 days, costs approximately USD$84,000 (often not covered by insurance), and lacks the scientific research and integrity of evidence based methods.

The Stanford group concluded that when "compared to costs described for adults with AN, adolescent treatment costs appear to be lower when families are used effectively to aid in treatment."

Introduction

2008-06-27T20:15:00.000-04:00

Hello everyone!

I am delighted and honored to be asked by Laura Collins to blog about eating disorders research for FEAST. I am not the parent of someone with an eating disorder- rather, I am the sufferer herself. One who is on her way to recovery with the help of her parents and a modified Maudsley approach.

I am also a science writer by profession. I have written two books on eating disorders: a memoir, Running on Empty, and a self-help book for teens and their parents called Next to Nothing. I have a Master's of Public Health in epidemiology from the University of Michigan, and I recently graduated from Johns Hopkins University with an MA in science writing (master's degrees- collect them all!).

I have written a variety of freelance pieces for such magazines as the Johns Hopkins Public Health Magazine, ScienceNOW, Eating Disorders Today, and the Etsy Storque. I currently work at Chemical and Engineering News as an editorial intern. After that, who knows.

Besides that, I also have a blog on eating disorders called ED Bites. Though I do blog about research there, it's not always my focus, and nor is my audience parents. There will likely be some cross-posting between the two blogs, especially if I think an article is generally useful.

If you have any questions, suggestions for articles, or comments, please email me at carrie [AT] edbites [.] com or post them in the "comments" section.

I'm very excited to work with FEAST and I hope to meet some of you at the NEDA conference in Austin this September.