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Wired for Hunger

Posted Jan 11 2010 3:50pm
A post on the DANA Foundation blog, titled "Wired for Hunger," looks at obesity, how the body regulates hunger and satiety, and what happens when these systems malfunction. But that's not the real interesting part. The interesting part was the sidebar on anorexia. It was both interesting and scientifically astute, with some testable hypotheses and potential interventions for anorexia. I'm copying it in its entirety here because I really think its worth reading.

Anorexia Nervosa: A Mortal Clash between Reward and Hunger

Few disorders reveal the power of the brain’s cognitive circuitry more clearly than anorexia nervosa, a psychiatric disorder characterized by extreme undereating, loss of body weight, hyperactivity and hypothermia. Compared with other psychiatric conditions, this disorder has the highest mortality rate. We theorize that, in cases of anorexia nervosa, the brain’s ancient evolutionary wiring for adapting happily to low food availability is inappropriately activated and finds itself in a life-threatening battle with other brain signals demanding action to obtain nourishment.

One clue to the intensity of this clash is the elevated level of physical activity in patients with anorexia nervosa, a symptom that people have reported for more than 100 years. Several studies have established a relationship between obsessive-compulsive characteristics and exercise frequency in women with strenuous daily exercise routines and in hospitalized female patients with anorexia nervosa.16 In the patient group, preoccupation with weight was associated with both the frequency of exercise and pathological attitudes toward it. Addictive and obsessive-compulsive personalities contributed to excessive exercise because of their obligatory, pathological thoughts promoting it. Among anorexia nervosa patients, those who exercise excessively have more bulimic symptoms, higher levels of general psychopathology about eating and a greater degree of body dissatisfaction, anxiety, somatization (physical symptoms with a psychological origin), depression and irritability.

Scientists view the tendencies toward mental alertness and continued normal-to-high activity levels (despite insufficient nutrition and weight loss) as being relatively unique to anorexia nervosa patients, versus individuals who experience semi-starvation due to causes such as illness, chemotherapy or famine. For both of these tendencies, the most plausible explanation is activation of evolutionarily old circuitry leading to reward upon reduced energy intake.

A final clue is another characteristic of anorexia nervosa patients: 90 percent are women, mainly in their late teens. This leads us to propose that a cellular mechanism, in association with the changing hormonal milieu that is characteristic of anorexia nervosa patients, unifies and orchestrates activation of key brain circuits, which in turn leads to the behavioral and endocrine manifestation of anorexia nervosa. Our hypothesis is that anorexia nervosa occurs following shifts in the circulating hormones ghrelin, leptin and estradiol, which alter key groups of neurons. These alterations bring about sex-specific structural and functional changes in particular circuits of the midbrain that transmit the chemical dopamine to communicate. Dopamine then triggers a reward response in the prefrontal cortex and hypothalamus to undereating and overexercise.

We further hypothesize that rolling back this shift in reward response could reverse anorexia nervosa, and that either eliminating ghrelin signaling or suppressing the number of available long-chain free fatty acids in the brain could accomplish this. Neuronal cells normally activated by ghrelin use these acids for energy; thus, eliminating the fatty acids would silence the ghrelin-activated neuronal population. Patients who received controlled leptin and estrogen replacement therapy also might see their anorexic symptoms diminish. Moreover, we predict that if doctors help at-risk patients maintain estradiol and/or leptin levels during the initial phase of disease, the patients will be less likely to undergo the shift in reward responses that leads to anorexia nervosa.

Thoughts?
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