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BNL Addiction SymposiumAbstract DetailsFebruary 16, 2007, San Francisco, CA | Symposium Home Similarity of overeating behavior and drug addictionAuthors: Gene-Jack Wang, Nora D Volkow, Joanna S. Fowler The increasing number of obese individuals in the US and in many countries in the world adds urgency to the need to understand the mechanisms underlying pathological overeating. There is mounting evidence from our research at Brookhaven National Laboratory and from others that similar brain circuits are disrupted in drug addiction and in obesity. Our studies using positron emission tomography (PET) implicate the involvement of brain dopamine in normal and pathological food intake in humans. In one study of normal-body-weight fasting subjects, the presentation of food that could not be consumed was associated with increases in striatal extracellular dopamine, a neurotransmitter known to play a role in motivation as well as in experiencing reward and pleasure.. Since the research subjects experienced no reward or pleasure from eating the food, this finding provides evidence for the involvement of dopamine in the non-hedonic motivational properties of food. Additional PET findings may help to explain certain similarities between overeating in obese individuals and the loss of control and compulsive drug-taking behavior observed in drug-addicted subjects. For example, in pathologically obese subjects, we found reductions in striatal dopamine D2 receptors similar to that observed in drug-addicted subjects. We postulated that decreased levels of dopamine receptors predisposed subjects to search for strongly rewarding reinforcers; that is, drug-addicted subjects seek the drug whereas obese subjects seek food as a means to temporarily compensate for decreased sensitivity of their dopamine-regulated reward circuits. Our imaging studies have also shown that metabolic activity in the orbitofrontal cortex (OFC), a part of the brain that is key to controlling and planning behavior, is in part regulated by dopamine activity. In drug-addicted subjects, lower striatal dopamine D2 receptor levels were associated with lower metabolism in the OFC. Lower activity in this region could indicate a reduced ability to plan or control behavior, which has been implicated in the compulsive behavioural characteristics of drug-addictive states. Additionally, in normal-body-weight fasting subjects, food presentation increased metabolism in OFC, which was significantly associated with the perception of hunger and the desire for food. Such changes in perception and desire could explain the deleterious effects of constant exposure to food stimuli (e.g., advertisements and food displays) in overeating. In another study in obese subjects implanted with a gastric stimulator, which induces stomach expansion via electrical stimulation of the vagus nerve, we found the gastric stimulation increased metabolism in OFC, striatum, and hippocampus. The activation in the hippocampus during gastric stimulation is associated with a sensation of fullness. These regions are involved with self-control, motivation, and memory, respectively, and were previously shown to be involved in drug craving in addicted subjects. This finding suggests that similar brain circuits underlie the enhanced motivational drive for food (and for drugs) seen in obese (and drug-addicted) subjects. Different from drug-addicted subjects, obese subjects have increased metabolism in the somatosensory cortex when compared with control subjects, making them more sensitive to the sensory properties of food. In the case of obesity the reduction in dopamine D2 receptors coupled with the enhanced sensitivity to food palatability makes food their most salient reinforcer, putting them at risk for food over-consumption. . In summary, the studies from our laboratory provide evidence that multiple but similar brain circuits (reward, motivation, learning, inhibitory control) are disrupted in drug addiction and obesity. The results implicate the need for a multimodal approach in the treatment of obesity.
Last Modified: January 31, 2008 |