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Bulimia is a serious disorder, and effective treatment remains elusive. Research on a new treatment for bulimia, stimulation of the vagus nerve (vagal nerve stimulation), may provide a broad therapy so that more individuals can recover from this debilitating disorder.
Currently bulimia nervosa is a very difficult disease to treat with a small chance of successful recovery. Studies have shown that bulimia nervosa becomes chronic in a substantial number of patients with this disorder, which creates a need for long-term successful treatment. It has been found that 20 to 50 percent of patients with bulimia nervosa will have symptoms even five years after some form of treatment. Also, with many patients all forms of current treatment have been unsuccessful. Given the detrimental effects that bulimia nervosa has on the body, new research is being conducted to see if there is a physiological mechanism that perpetuates the disorder. Currently researchers at the University of Minnesota, Twin Cities, are conducting research on the vagus nerve to see if there is a possibility of retraining the vagus and thereby reducing bulimic episodes/ behaviors.
The Vagus nerve is cranial nerve 10 of the 12 cranial nerves. In latin, vagus means "wandering". It got this name because it splits off and connects to many organs in the gut including the heart, lungs, kidney, large intestine, small intestine, and liver.
The underlying mechanism that perpetuates bulimia nervosa is currently unknown. Research performed by Faris et al. (2000) was initiated by two particular facts for the possible involvement of the afferent vagal circuits in the perpetuation of bulimia nervosa. The first indication that the afferent vagal circuits were involved in bulimia nervosa was that patients lacked the ability to know/ feel when they had been satisfied or disgusted (satiety) by the food they had eaten. Also, since patients with bulimia nervosa lack normal satiety they have difficulty/inhibiting eating. Hence, patients need to eat more to be satisfied by a meal or reach fullness. Satiation is mainly affected by the vagus nerve, which sends information from the subdiaphramatic region to the brain. Stimulation of the vagus nerve (endogenously or exogenously) lets the patient know when they are satisfied by the food they have eaten or when they have eaten too much.
The second indication that the vagus nerve plays a role in the perpetuation of bulimia nervosa is that patients have a high pain threshold. Pain can be modulated by the vagus nerve stimulation. Hence, it has been found that an increase in vagus nerve activity produces and inability for the vagus nerve to send information about satiety to the brain as effectively. Hence, the ability for the brain to respond to a meal appropriately is compromised by increased vagal activity.
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