Eugene, OR, USA. Obese individuals have fewer pleasure receptors and overeat to compensate, according to new research which provides evidence of the vicious cycle created when an obese individual overeats to compensate for reduced pleasure from food.

This overeating may further weaken the responsiveness of an obese individual's pleasure receptors (hypofunctioning reward circuitry), further diminishing the rewards gained from overeating. Food intake is associated with dopamine release. The degree of pleasure derived from eating correlates with the amount of dopamine released.

The evidence shows obese individuals have fewer dopamine (D2) receptors in the brain relative to lean individuals. People with fewer of the dopamine receptors need to take in more of a rewarding substance — such as food or drugs — to get an effect other people get with less. Thus, there is a corresponding compensation for the reward deficit.

The study was led by Eric Stice, a University of Texas at Austin senior research fellow and a senior scientist at the Oregon Research Institute (ORI). Stice and his colleagues published their findings in The Journal of Neuroscience.

Stice has studied eating disorders and obesity for 20 years. This research has produced several prevention programs that reliably reduce risk for onset of eating disorders and obesity.

"Although recent findings suggested that obese individuals may experience less pleasure when eating, and therefore eat more to compensate, this is the first prospective evidence to show that the overeating itself further blunts the award circuitry. The weakened responsivity of the reward circuitry increases the risk for future weight gain in a feed-forward manner. This may explain why obesity typically shows a chronic course and is resistant to treatment."

Using Functional Magnetic Resonance Imaging (fMRI), Stice's team measured the extent to which a certain area of the brain (the dorsal striatum) was activated in response to the individual's consumption of a taste of chocolate milkshake (versus a tasteless solution). Researchers tracked participants' changes in body mass index over six months.

Results indicated those participants who gained weight showed significantly less activation in response to the milkshake intake at six-month follow-up relative to their baseline scan and relative to women who did not gain weight.

"This is a novel contribution to the literature because, to our knowledge, this is the first prospective fMRI study to investigate change in striatal response to food consumption as a function of weight change," said Stice. "These results will be important when developing programs to prevent and treat obesity."

Citation
Weight Gain Is Associated with Reduced Striatal Response to Palatable Food. Eric Stice, Sonja Yokum, Kenneth Blum, and Cara Bohon. The Journal of Neuroscience 2010; 30(39): 13105-13109. doi:10.1523/JNEUROSCI.2105-10.2010

Abstract

Consistent with the theory that individuals with hypofunctioning reward circuitry overeat to compensate for a reward deficit, obese versus lean humans have fewer striatal D2 receptors and show less striatal response to palatable food intake. Low striatal response to food intake predicts future weight gain in those at genetic risk for reduced signaling of dopamine-based reward circuitry. Yet animal studies indicate that intake of palatable food results in downregulation of D2 receptors, reduced D2 sensitivity, and decreased reward sensitivity, implying that overeating may contribute to reduced striatal responsivity. Thus, we tested whether overeating leads to reduced striatal responsivity to palatable food intake in humans using repeated-measures functional magnetic resonance imaging. Results indicated that women who gained weight over a 6 month period showed a reduction in striatal response to palatable food consumption relative to weight-stable women. Collectively, results suggest that low sensitivity of reward circuitry increases risk for overeating and that this overeating may further attenuate responsivity of reward circuitry in a feedforward process.

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