More Light on Addictive-Like Eating Disorders

Brain studies show a link between substance abuse and addictive food behaviors

Reprinted from Eating Disorders Review
May/June 2011 Volume 22, Number 3
©2011 Gürze Books

A new study using functional magnetic resonance imaging (fMRI) has shown that women with addictive-like eating disorders have neural activity similar to that of substance abusers.

In a small study of 48 healthy young women (mean age: 20), Ashley Gearhardt and colleagues at the Department of Psychology at Yale University found that women with higher food addiction scores had greater activity in brain regions associated with reward than did women with lower scores (Arch Gen Psychiatry 2011; Apr 4 [Epub ahead of publication].

The researchers had noted from prior research that an addictive-like process has been implicated in the development of obesity. Food and drug use both result in dopamine release in the mesolimbic regions of the brain and the degree of dopamine release correlates with subjective reward from both food and drug use. The authors hypothesized that higher scores on a food addiction scale (the Yale Food Addiction Scale) would be associated with patterns of neural activation similar to those of substance dependence.

The women, who were recruited for a long-term healthy weight maintenance trial, had body mass indexes (BMIs, kg/m2) ranging from normal to obese (24 kg/m2 to 40 kg/m2). Each woman underwent fMRI scans as she was exposed to two conditions: first, during anticipation of consuming a rich chocolate milkshake versus a tasteless control solution shake, and second, while consuming the tasty milkshake versus the tasteless control shake. When the women actually got to drink the milkshake, the researchers found they had reduced activation of inhibitory brain areas, as seen on fMRI scans.

When the subjects anticipated drinking the milkshakes, food addiction scores correlated with greater activity in the anterior cingulate cortex, medial orbitofrontal cortex, and the amygdale. The anterior cingulate cortex and the orbitofrontal cortex have both been implicated in motivation to eat, as well as with intake of drugs in patients with substance abuse, and the amygdala is also linked to increased motivation to eat.

Women with higher food addiction scores also had greater activation in other brain regions associated with anticipation of reward, including the dorsolateral prefrontal cortex, and the caudate. Yet, when the women actually drank the milkshake, there was less activation in the lateral orbitofrontal cortexan area associated with inhibitory control and the ability to suppress previously rewarded responses. The authors surmised that the reduced activation might be related to less inhibitory control during intake of palatable food or to a reduced satiety response during palatable food intake,

The study showed no significant associations between food addiction scores and BMI. The authors concluded that compulsive food consumption may be partly driven by enhanced anticipation of the rewarding properties of food, and that eating may override the desire to limit calories, leading to disinhibited food consumptions.

The study had some limitations, including exclusion of persons with eating disorders and Axis I psychiatric disorders, so few of the women met the criterion of clinically significant distress or impairment on the Yale Food Addiction Scale, which is required for a diagnosis of food addiction. Thus, the authors recommend that future studies include participants with more severe food addiction scores. In addition, the team did not attempt to measure hunger (participants were asked to refrain from eating 4 to 6 hours before their fMRI session); fasting and hunger are associated with similar patterns of neural response, which might also affect the results.

Despite the small size of the study and its limitations, the results did provide an early window into neural patterns of addictive-like eating behavior and substance dependence.

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