RT Journal A1 Gearhardt AN, Yokum S, Orr PT, Stice E, Corbin WR, Brownell KD T1 NEural correlates of food addiction JF Archives of General Psychiatry JO Archives of General Psychiatry YR 2011 FD August 1 VO 68 IS 8 SP 808 OP 816 DO 10.1001/archgenpsychiatry.2011.32 UL http://dx.doi.org/10.1001/archgenpsychiatry.2011.32 AB Context  Research has implicated an addictive process in the development and maintenance of obesity. Although parallels in neural functioning between obesity and substance dependence have been found, to our knowledge, no studies have examined the neural correlates of addictive-like eating behavior.Objective  To test the hypothesis that elevated“food addiction” scores are associated with similar patterns of neural activation as substance dependence.Design  Between-subjects functional magnetic resonance imaging study.Setting  A university neuroimaging center.Participants  Forty-eight healthy young women ranging from lean to obese recruited for a healthy weight maintenance trial.Main Outcome Measure  The relation between elevated food addiction scores and blood oxygen level–dependent functional magnetic resonance imaging activation in response to receipt and anticipated receipt of palatable food (chocolate milkshake).Results  Food addiction scores (N = 39) correlated with greater activation in the anterior cingulate cortex, medial orbitofrontal cortex, and amygdala in response to anticipated receipt of food (P < .05, false discovery rate corrected for multiple comparisons in small volumes). Participants with higher (n = 15) vs lower (n = 11) food addiction scores showed greater activation in the dorsolateral prefrontal cortex and the caudate in response to anticipated receipt of food but less activation in the lateral orbitofrontal cortex in response to receipt of food (false discovery rate–corrected P < .05).Conclusions  Similar patterns of neural activation are implicated in addictive-like eating behavior and substance dependence: elevated activation in reward circuitry in response to food cues and reduced activation of inhibitory regions in response to food intake.