October 4, 2006.
Researchers at the U.S. Department of Energy's Brookhaven National Laboratory report food to be a form addiction for obese people. They have proved the interaction between the brain, stomach and emotions can cause overeating and obesity.
To define brain circuits that motivate the desire to overeat in the obese, the scientists have implanted a device that stimulates the stomach. They observed the reaction of brain to the "fullness" messages sent by the device. It has been found that the affected circuits are the same that cause addicted individuals to crave drugs. The critical role of these circuits in the connection between eating behavior and soothing negative emotions has also been verified. The results of the investigation were published in the Proceedings of the National Academy of Sciences, October 17, 2006 and online in PNAS Early Edition the week of October 2.
Lead author, Gene-Jack Wang, Brookhaven Lab's Center for Translational Neuroimaging, said the study gave some explanation to the connection of the body and brain and how was it related to obesity. According to Wang, they have managed to turn 'off' the brain's desire to continue eating by stimulating the process that takes place when the stomach is full.
Seven obese individuals with gastric stimulators implanted for one to two years were kept under observation. Wang and colleagues studied their brain metabolism. The stimulator principle of operation is the same as of a pacemaker: the vagues nerves, affected by low levels electrical stimulation, cause the stomach to expand and produce peptides that send messages of "fullness" to the brain.
Researches have observed the reduction of the desire to eat. The investigation provides the first direct evidence of which brain regions are involved in this response. It opens new territory in understanding of how eating behavior is connected with satiety signals sent by the stomach.
Participants in the study underwent two separate positron emission tomography (PET) brain scans. They were held two weeks apart: one with the gastric stimulator on, the other with the stimulator off. The patients were not aware of their implanted device was on or off. To have a chance to monitor brain metabolism participants received the injections of a radioactively labeled form of glucose, which the scanner could track.
Wang and his group have found significant changes in metabolism in brain regions associated with controlling emotions. They were induced by the implanted gastric simulators, which showed an effective reduction of the desire to eat.
18 percent rise of metabolism has been revealed in the hippocampus during gastric stimulation. The hippocampus is considered to be linked with learning and memory, emotional behavior and processing of sensory and motor impulses. It is in the most part responsible for the retention of memories related to prior drug experiences in addicted individuals. Hippocampal activation might also stimulate the memories of satiety in the obese.
The implanted stimulators affected the brain circuits in the orbitofrontal cortex and striatum by sending messages of satiety. These areas of brain have been linked to craving and desire for drugs in drug-addicted patients.
To determine the correlation between eating behaviors and areas of brain stimulated by the implanted device, participants answered the questionnaire at each brain scanning session. The worksheet measured three aspects of eating behavior: uncontrolled eating, cognitive restraint and emotional eating. It was found that scores on a measure of self-described "emotional eating" during gastric stimulation were 21 percent lower than when the stimulator was off.
According to Gene-Jack Wang, the study provides evidence of the connection between the hippocampus, the emotions, and the desire to eat. The mechanisms by which obese people use food to soothe their emotions now can be observed in details. Wang believes the further studies of the new pathway would determine implications for treating or preventing obesity.
