Neural Correlates of Food Addiction

Abstract

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, 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 fMRI study. Participants Forty-eight healthy adolescent females 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 fMRI 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 (ACC), medial orbitofrontal cortex (OFC), and amygdala in response to anticipated receipt of food (P <0.05, false-discovery rate (FDR) corrected for multiple comparisons in small volumes). Participants with higher (n=15) versus lower (n=11) food addiction scores showed greater activation in the dorsolateral prefrontal cortex (DLPFC) and the caudate in response to anticipated receipt of food, but less activation in the lateral OFC in response to receipt of food (pFDR <0.05). 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.

Role of Orexin-1 Receptor Mechanisms on Compulsive Food Consumption in a Model of Binge Eating in Female Rats

“…In keeping with the idea that Orexin-1 receptor mechanisms in binge eating in rats L Piccoli et al neural systems that motivate and reinforce drug abuse may also underlie behaviors associated with food seeking and intake (Gearhardt et al, 2011b), this study investigated the ability of OXR antagonist to block BE episodes and to evaluate the involvement of OX 1 and OX 2 mechanisms in the control of BE episodes.…”

“…Neural systems that motivate and reinforce drug abuse have also been proposed to underlie behaviors associated with compulsive food seeking and food intake (Johnson and Kenny, 2010;Hoebel, 1985;Volkow and Wise, 2005;Corwin et al, 2011;Gearhardt et al, 2011b;Wang et al, 2011). These findings raise the question of whether the OX system may also have a role in eating disorders characterized by compulsive binge-type episodes, such as bulimia nervosa and BED.…”

Fat brains, greedy genes, and parent power: A biobehavioural risk model of child and adult obesity

“…the tendency for restraint to break down when confronted by emotional or external cues to eat) has been associated with lesser pre-meal ACC responses to visual food versus non-food cues , and scores on food addiction (i.e. a pattern of compulsive eating typifi ed by tolerance, withdrawal and loss of control) have been associated with greater medial orbitofrontal cortex (OFC), amygdala and ACC responses to anticipated receipt of a milkshake, and lesser activation in the lateral OFC in response to actual receipt (Gearhardt et al, 2011).…”

Co-occurring weight problems among children with attention deficit/hyperactivity disorder: the role of executive functioning

“…22 For example, research has demonstrated diminished striatal dopamine release after eating desirable food, 23 and abnormalities in dopaminergic response to food cues and actual food consumption in adults with food addiction. 24 Diminished dopamine receptor-binding capacity in the hypothalamus, which controls satiety and hunger, has been observed in individuals with ADHD, 25 suggesting a direct causal link between ADHD and eating patterns, although research with children is limited. Hence, initial evidence suggests that dopaminergic dysfunction leads to impairment in reward processing that promote both obesity and ADHD.…”