The idea that obese people eat too much because they find food more palatable than lean people do has gained support from a new brain-imaging study at the U.S. Department of Energy’s Brookhaven National Laboratory. The study published in the July 2, 2002, issue of the journal NeuroReport, reveals that the parts of the brain responsible for sensation in the mouth, lips, and tongue are more active in obese people than in normal-weight control subjects.
“This enhanced activity in brain regions involved with sensory processing of food could make obese people more sensitive to the rewarding properties of food, and could be one of the reasons they overeat,” said Brookhaven physician Gene-Jack Wang, lead author of the study.
Wang acknowledges that obesity is a complex disease with many contributing factors, including genetics, abnormal eating behavior, lack of exercise, and cultural influences, as well as cerebral mechanisms, which are not yet fully understood. In a recent study, he and his team found that obese people have fewer brain receptors for dopamine, a neurotransmitter that helps produce feelings of satisfaction and pleasure, implying that obese people may eat to stimulate their underserved reward circuits, just as addicts do by taking drugs.
In that study, overall brain metabolism did not differ between obese and normal-weight controls. But because the sensory appeal of food can be so important in triggering the urge to eat, Wang and his team wondered whether obese people might have enhanced metabolic activity in specific brain regions, particularly those involved in the sensory processing of food.
To measure regional brain metabolism, the scientists used positron emission tomography (PET) after injecting volunteers (10 severely obese and 20 normal controls) with a radioactively labeled form of glucose, the brain’s metabolic fuel. Known as FDG, this radiotracer (invented at Brookhaven) acts like glucose in the brain, concentrating in regions where metabolic activity is highest. The PET scanner picks up the radioactive signal to reveal where the FDG is located.
The scientists used a computer program to average the PET data from the subjects within each group, and then compared the obese subjects’ average with the normal subjects’ result. The program produced three-dimensional images highlighting areas where the obese group had higher metabolic activity than the normal-weight group.
The scientists then superimposed these images onto a magnetic resonance image (MRI) of the whole brain, as well as a diagram of the brain’s somatosensory cortex, known as a homunculus. A homunculus graphically illustrates the relative number of sensory nerves innervating various parts of the body as well as where the input from these nerves is received on the somatosensory cortex.
The overlapping images revealed “hot spots” — indicating obese subjects’ higher metabolic activity — in the regions of the parietal cortex where somatosensory input from the mouth, lips, and tongue is received. This is also an area involved with taste perception.
“The enhanced activation of these parietal regions in obese subjects is consistent with an enhanced sensitivity to food palatability, which is likely to increase the rewarding properties of food,” Wang said.
Taken together with the earlier results on deficient reward circuits, this enhanced sensitivity could account for the powerful appeal and significance that food has for obese individuals.
The findings also suggest that pharmacological treatments known to decrease palatability might be useful along with behavioral therapies in reducing food intake in obese subjects.