Noted brain experts Richard Wurtman and Judith Wurtman conducted experiments with CCO (carbohydrate-craving obesity) patients. Their work demonstrated how the urge to consume carbohydrates strikes predictably during the late afternoon. But why should this be so? If a person has a disorder that compels her to eat huge quantities of food, why should her appetite be greater at certain times of day? And why is it limited to a certain type of macronutrient? Not all of the answers are in yet. However, some evidence points to the neurotransmitter serotonin-or rather, a defect in serotonin secretion-as one possible source of the problem.
A normal person who feels the urge to eat something sweet might be satisfied with a couple of cookies or a candy bar. In contrast, a carbohydrate craver continues to eat beyond the point of satisfaction. As we learned earlier, serotonin usually acts to suppress eating. The Wurtmans believe that carbohydrate-craving behavior suggests something has gone wrong with the feedback loop that signals the brain when enough food has been taken in.
There’s another level to the problem as well. When asked why they succumbed to such dangerous eating practices, carbohydrate-craving people reported that they weren’t interested in the taste of the food. Instead they ate as a means of fending off tension, anxiety, or mental fatigue. In other words, carbohydrate cravers seem to use food as a kind of self-prescribed regimen of antidepressant therapy. Earlier we saw how carbohydrates lead to increased serotonin levels. Could a defect in the serotonin system be a common link between these disorders?
Knowing that a faulty serotonin system may underlie certain kinds of abnormal eating has led to the use of medications to correct the problem. A chemical called d-fenfluramine, for example, acts as a kind of biological boxing coach. It calls on serotonin to get out there and fight by triggering its release from nerve cells. Then d-fenfluramine prolongs the bout by blocking reabsorption of serotonin back into the cell-in a sense, keeping the boxer from returning to his corner before the fight is over. The popular antidepressant Prozac (fluoxetine) also increases serotonin levels by blocking the reabsorption of serotonin by the nerve cells.
Through this one-two punch, d-fenfluramine helps serotonin do the job it was designed for: control appetite. Use of this and other similar compounds can help some carbohydrate-craving patients enjoy more normal moods and in some cases lose weight. There has also been some success in using these medications for PMS and SAD. Recent research in patients with PMS has also shown that consumption of high-carbohydrate meals (which increases serotonin) can help improve premenstrual depression, tension, and fatigue.
Eating is not just a simple process. A complex network of signals exists between the brain and the rest of the body. Some of these signals arise from within. Others- anything from the amount of daylight outside to a friend’s invitation to go and grab a burger-come from the outside world.
These signals trigger the release of biochemicals that stimulate appetite. The digestive organs respond to what we eat by releasing still more chemical messengers that report to the brain. The brain processes the information and issues orders to stop, continue, or eat something different next time.
Although social cues play a role, eating is largely a self-sustaining physical process. Disruptions can occur at any point in the system. There may be insufficient supplies of a certain brain chemical or a defect in an organ’s ability to respond to a neurotransmitter’s message. Fortunately, our growing knowledge of how physical problems contribute to eating disorders points the way to new and effective biological treatments.
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