Having experienced anorexia nervosa firsthand, I’ve always wondered what goes on in my brain to make it so hard to gain weight. Call all it brainwashing. Now comes a review of the brain circuitry underlying the drives, thoughts and urges of anorexia, with all their fury.
This month, Walter Kaye, at the University of California San Diego, has published a fantastic and complex model of what might be happening based on studies of both women who are suffering from anorexia and those who have recovered. To simplify:
●Certain individuals are born with a proclivity toward the disease – we’ve got traits such as a powerful urge to avoid harm, perfectionism and a warped sense of inner awareness (for example, we don’t feel hunger or deprivation the same as others).
●Starving further alters brain and body chemistry to exacerbate the symptoms of the disease.
●The combination of trait and behaviors (self-starvation, overexercise, etc.) create an endless spiral of destruction.
That’s what happens on the surface. “Peeking under the hood,” people with anorexia show two altered brain circuits: the serotonin system -- a controller of mood—and dopamine – an orchestrator of reward.
Detailing the serotonin system, here’s Kaye’s diagram:
Individuals with anorexia are either born oversensitive toward serotonin (5-HT) or become that way after dieting. Biochemically, we have too many copies of one receptor for serotonin (5HT1A) and not enough of another receptor (5HT2A).
At the same time, we have too much serotonin hovering about the synapses of nerve cells. That causes bad mood, poor judgment (i.e. about self-care) and an irrational terror of trying new things (for fear of harm or paying consequences.
By dieting, we decrease the serotonin stores near the synapses because certain foods contain a chemical – known as tryptophan—which the body uses to make serotonin. Less tryptophan-containing foods in the gut, less serotonin 5HT in the brain. Therefore, dieting boosts mood. But only in the short term.
Brain cells compensate for decreased serotonin by making more 5HT1A receptors. That causes mood to turn dark again, and so we starve to try to lighten it. The brain makes more receptors and so on in a downward cycle.
At the same time, continued starvation also depletes levels of a stress hormone, known as CRH, and endorphins which give that feeling of “high.”(Think exercise, which increases endorphins.) Again, mood worsens, and we diet more to try and feel better. And so the cycle of dieting, weight loss and mood swings turn viscous.
Forced-eating feels horrid to a person with anorexia because it ups the levels of serotonin, and does so at a time when we already have too many receptors for the neurotransmitter. Too much serotonin and too many receptors mean an intensely bad mood. Thus, forced eating, at first, feels like hell…until the brain cells and their receptors adjust to the heightened levels of serotonin and balance again.
All this means, that eating in recovery may be hard, but absolutely necessary to set the brain right. The sooner the better, because long term problems with this circuit can become irreversible. Bottom line, if you are in recovery from anorexia and suffering, it will feel better, eventually.
Another key point, Kaye also showed that people with anorexia don’t feel reward (about food, for example) in the moment. Instead, we plan to the future, analyze and think mainly of long term consequences (i.e. if I eat this cake now, I will feel terrible tomorrow). Biochemically, our dopamine systems are out of whack as measured by an imbalance in dopamine receptors D2/D3.
In the short term, it might be possible to use that alteration as an asset in recovery. If you can see a “long term consequence” as a better life that involves pleasure, then you can aim for that strategically, while you are getting through the bad mood phase, which may take months or years to complete. Another way to say it is that if you driven to diet, like I am, you can drive yourself to recovery with equal ambition. The other hope is that all this brain work by scientists will lead toward drugs that target the faulty receptors and help us achieve balance in the short and longer term.
Thanks to Dr. Kaye for all this work. It helps to know it’s not all “in our heads.”

I have found stark connections between my eating disorder and my other comorbid issues: they all involve seratonin and dopamine. ADD? Fibromyalgia? Sleep issues? All the same.
I think the question we should be asking is, "Why are so many people being born with dysfunctional seratonin?"
Posted by: Yum | August 21, 2009 at 07:36 AM