The cerebral mechanisms underlying the behaviours that lead to pathological overeating and obesity are poorly understood. Dopamine, a neurotransmitter that modulates rewarding properties of food, is likely to be involved. To test the hypothesis that obese individuals have abnormalities in brain dopamine activity we measured the availability of dopamine D₂ receptors in brain.

Brain dopamine D₂ receptor availability was measured with positron emission tomography (PET) and [C-11]raclopride (a radioligand for the dopamine D₂ receptor). Bmax/Kd (ratio of the distribution volumes in striatum to that in cerebellum minus 1) was used as a measure of dopamine D₂ receptor availability. Brain glucose metabolism was also assessed with 2-deoxy-2[¹⁸F]fluoro-D-glucose (FDG).

Striatal dopamine D₂ receptor availability was significantly lower in the ten obese individuals (2·47 [SD 0·36]) than in controls (2·99 [0·41]; p<0·0075). In the obese individuals body mass index (BMI) correlated negatively with the measures of D₂ receptors (r=0·84; p⩾0·002); the individuals with the lowest D₂ values had the largest BMI. By contrast, neither whole brain nor striatal metabolism differed between obese individuals and controls, indicating that striatal reductions in D₂ receptors were not due to a systematic reduction in radiotracer delivery.

The availability of dopamine D₂ receptor was decreased in obese individuals in proportion to their BMI. Dopamine modulates motivation and reward circuits and hence dopamine deficiency in obese individuals may perpetuate pathological eating as a means to compensate for decreased activation of these circuits. Strategies aimed at improving dopamine function may be beneficial in the treatment of obese individuals.