Monday, April 04, 2011

Food Addiction Has Correlates in Neural Activity


In the current issue of JAMA's Archives of General Psychiatry, researchers report finding neural activity linked to food addiction. The basic response is similar to other addictions - there is more activity in the reward circuitry in response to food cues and less activity in the inhibitory circuits in response to food intake (eating the desired food makes it easier to eat even more of the desired food, which is how food addiction leads to obesity).

The downside to this finding (which has been shown in other studies) is that it will tempt drug companies to seek a pharmacological treatment and/or encourage psychiatrists to prescribe drugs the same way they do for other addictions, like alcoholism.

The real problem is more often than not (thyroid is a rare cause of obesity) that the person is self-medicating (with food), which is true of most other addictions, too. We need to stop focusing on diet and exercise for the folks who are most at risk and deal with the wounding or trauma that is being buried beneath the fat and drugged with the food intake.

Reference:

Gearhardt, AN, Yokum, S, Orr, PT, Stice, E, Corbin, WR, & Brownell, KD. (2011, April 4). Study Identifies Neural Activity Linked to Food Addiction. Arch Gen Psychiatry, doi:10.1001/archgenpsychiatry.2011.32

Here is the abstract for the article.

Neural Correlates of Food Addiction

Ashley N. Gearhardt, MS, MPhil; Sonja Yokum, PhD; Patrick T. Orr, MS, MPhil; Eric Stice, PhD; William R. Corbin, PhD; Kelly D. Brownell, PhD

Arch Gen Psychiatry. Published online April 4, 2011. doi:10.1001/archgenpsychiatry.2011.32

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.

The study is better explained by the press release.
Study Identifies Neural Activity Linked to Food Addiction

CHICAGO—Persons with an addictive-like eating behavior appear to have greater neural activity in certain regions of the brain similar to substance dependence, including elevated activation in reward circuitry in response to food cues, according to a report posted online today that will appear in the August print issue of Archives of General Psychiatry, one of the JAMA/Archives journals.

"One-third of American adults are now obese and obesity-related disease is the second leading cause of preventable death. Unfortunately, most obesity treatments do not result in lasting weight loss because most patients regain their lost weight within five years," the authors write. "Based on numerous parallels in neural functioning associated with substance dependence and obesity, theorists have proposed that addictive processes may be involved in the etiology of obesity. Food and drug use both result in dopamine release in mesolimbic regions [of the brain] and the degree of release correlates with subjective reward from both food and drug use." The researchers add that to their knowledge, no studies have examined the neural correlates of addictive-like eating behavior.

Ashley N. Gearhardt, M.S., M.Phil., of Yale University, New Haven, Conn., and colleagues examined the relation between food addiction (FA) symptoms, as assessed by the Yale Food Addiction Scale (YFAS), with neural activation (measured via functional magnetic resonance imaging) in response to cues signaling impending delivery of a highly palatable food (chocolate milkshake) vs. a tasteless control solution; and consumption of a chocolate milkshake vs. a tasteless solution. The study included 48 healthy young women ranging from lean to obese recruited for a healthy weight maintenance trial.

The researchers found that food addiction scores correlated with greater activation in areas of the brain including the anterior cingulate cortex (ACC), medial orbitofrontal cortex (OFC), and amygdala in response to anticipated receipt of food. Participants with high vs. low FA demonstrated greater activation in the dorsolateral prefrontal cortex and caudate during anticipated palatable food intake and reduced activation in the lateral OFC during palatable food consumption.

"As predicted, elevated FA scores were associated with greater activation of regions that play a role in encoding the motivational value of stimuli in response to food cues. The ACC and medial OFC have both been implicated in motivation to feed and to consume drugs among individuals with substance dependence," the authors write. "In sum, these findings support the theory that compulsive food consumption may be driven in part by an enhanced anticipation of the rewarding properties of food. Similarly, addicted individuals are more likely to be physiologically, psychologically, and behaviorally reactive to substance-related cues."

"To our knowledge, this is the first study to link indicators of addictive eating behavior with a specific pattern of neural activation. The current study also provides evidence that objectively measured biological differences are related to variations in YFAS scores, thus providing further support for the validity of the scale. Further, if certain foods are addictive, this may partially explain the difficulty people experience in achieving sustainable weight loss. If food cues take on enhanced motivational properties in a manner analogous to drug cues, efforts to change the current food environment may be critical to successful weight loss and prevention efforts. Ubiquitous food advertising and the availability of inexpensive palatable foods may make it extremely difficult to adhere to healthier food choices because the omnipresent food cues trigger the reward system. Finally, if palatable food consumption is accompanied by disinhibition [loss of inhibition], the current emphasis on personal responsibility as the anecdote to increasing obesity rates may have minimal effectiveness," the researchers conclude.

Available to the media pre-embargo at www.jamamedia.org).


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