The face in the coffee beans

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

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

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)

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

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

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

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

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

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

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

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!

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

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!

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

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

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

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

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

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...

...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.