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.

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