Monday, December 21, 2009

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.

Tuesday, December 15, 2009

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.

Friday, October 9, 2009

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.

Thursday, September 24, 2009

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."

Monday, September 7, 2009

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:

" 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)

Monday, August 17, 2009

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.


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.

Tuesday, August 11, 2009

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!

Thursday, July 2, 2009

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

Friday, June 26, 2009

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.

Thursday, June 25, 2009

Sunday, May 24, 2009

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)

Tuesday, May 19, 2009

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)

Monday, April 13, 2009

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.

Thursday, April 2, 2009

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!

Wednesday, April 1, 2009

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.

Tuesday, March 24, 2009

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.

Thursday, March 19, 2009

Hypermetabolism: the basics

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

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

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!