COMMENTS: This describes a study (Neural Correlates of Food Addiction) that is first to compare brain activation patterns of “food addicts”. Other studies have looked at the brains of obese humans. Some the women in this study classified as food addicts were not obese. The results: brain activation of food addicts matches that of drug addicts. Here’s a very important quote:
“We already know what the imaging profile is for addictive behavior and what the profile is for the reward system, which is the dopamine system. What they’re really saying is that this is a nonspecific activation pattern that is not stimulus sensitive. No matter what the addiction, it’s going to affect the same areas.”
In other words, all addictions involve similar mechanisms and brain pathways, including porn addiction.
Imaging study first to assess neural correlates in food addiction, by Deborah Brauser
April 7, 2011 — Addictive-like eating behavior and substance dependence share similar patterns of neural activation, according to a new functional magnetic resonance imaging (fMRI) study, raising the possibility that the current emphasis on personal responsibility as the potential antidote to the obesity epidemic may be misguided.
After evaluating 48 healthy women, investigators found that food cues for a desirable product led to increased activity in the brain’s reward regions, including the dorsolateral prefrontal cortex and the caudate, whereas the response to food intake resulted in reduced activation of inhibitory regions.
“Our findings showed high reward-related activation in brain regions that are implicated in craving and enhanced motivation in a very similar manner to what you would typically expect to see with alcoholism or nicotine dependence,” lead author Ashley Gearhardt, MS, clinical psychology doctoral student involved with the Rudd Center for Food Policy and Obesity at Yale University in New Haven, Connecticut, told Medscape Medical News.
The investigators note that although previous studies have shown associations between obesity and substance dependence, this is the first to assess the neural correlates of food addiction behaviors.
“The findings support the theory that compulsive food consumption may be driven in part by an enhanced anticipation of the rewarding properties of food. Also, if palatable food consumption is accompanied by disinhibition, the current emphasis on personal responsibility as the antidote to increasing obesity rates may have minimal effectiveness,” they write.
“This is kind of a one-two punch that’s going on. In addition to an almost obsessive craving that is set off by food cues, such as through advertising or walking by a bakery, the biological region that houses the ability to have the willpower to not partake kind of goes offline,” added Ms. Gearhardt.
The study was published online April 4 in the Archives of General Psychiatry.
Milkshake Paradigm
Obesity is now the second leading cause of preventable death and affects a third of all adults living in the United States.
“Unfortunately, most obesity treatments do not result in lasting weight loss because most patients regain their lost weight within 5 years,” the investigators write.
For this study, the investigators evaluated data on 48 women (mean age, 20.8 years) of varying body types (mean body mass index, 28.0) who were enrolled in a healthy weight maintenance trial.
Food addiction symptoms were assessed for all participants by using the 25-item Yale Food Addiction Scale (YFAS). These symptoms were evaluated in relation to neural activity from fMRI during food cues (photos) signaling the impending delivery of a chocolate milkshake or a tasteless control solution, as well as during the actual intake of either drink.
“The milkshake paradigm was designed to examine activation in response to consumption and anticipated consumption of palatable food,” the researchers explain.
In response to anticipated delivery of the milkshake, the YFAS scores significantly correlated with activation in the left anterior cingulate cortex (ACC), left medial orbitofrontal cortex (OFC), and left amygdala (P < .05).
Women who had higher YFAS scores showed greater activation in the dorsolateral prefrontal cortex and the right caudate in response to cues of the anticipated palatable drink compared with those who had lower scores. However, they had less activation in the left lateral OFC in response to the actual receipt of the drink (both P < .05).
Longitudinal Study Needed
“The ACC and medial OFC have both been implicated in motivation to feed and to consume drugs among individuals with substance dependence. Elevated ACC activation in response to alcohol-related cues is also associated with reduced D2 receptor availability and increased risk for relapse,” write the investigators.
They note that the amygdala and caudate have also been implicated in drug cue reactivity and craving.
In addition, the investigators write that it was “interesting” that the YFAS scores were positively correlated with activation in the medial OFC during anticipation but were correlated negatively with lateral OFC activation during receipt. They suggest that this pattern may occur as participants’ desire for the reward decreases and their consumptive behavior then becomes inconsistent with their desires.
“Thus, lateral OFC activity occurs when the desire to stop eating is suppressed,” explain the researchers, noting that these types of patterns have also been found in substance dependence.
“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.”
However, Ms. Gearhardt reported that the study could not differentiate whether something was already going on in the brain that made certain people more susceptible to food triggers or if certain addictive foods are setting off the activity in the brain.
“We need to do a longitudinal study where we’d follow people before they have problems to see what comes first — the brain activation or the behavior. What we’ve seen commonly in addiction is a combination of the two.”
She reported that the investigators are working on a study that “explores what food addiction looks like on a widespread community scale.” In addition, they plan on looking at how food addiction may be playing a role in child obesity.
Biologic Proof
“We already know what the imaging profile is for addictive behavior and what the profile is for the reward system, which is the dopamine system,” Max Wiznitzer, MD, associate professor of pediatrics and neurology at Case Western Reserve University in Cleveland, Ohio, and a neurologist at UH Rainbow Babies and Children’s Hospital, told Medscape Medical News.
“What this paper stated was that the neuroimaging profile to some degree was correlated between food addiction scores and activation in certain areas of the brain that have been identified in the past with the addictive profile, ” added Dr. Wiznitzer, who was not involved in the research.
He noted that an interesting study point was that few of the participants met all the criteria for a full food addiction diagnosis.
“So these were conservative findings. This was not that severe a group, yet it suggests that the more you’re a foodie, the more likely you are to show this activation pattern. What they’re really saying is that this is a nonspecific activation pattern that is not stimulus sensitive. No matter what the addiction, it’s going to affect the same areas,” he said.
“Now that we know this, what is the clinical implication? There’s already a clinical scale that describes food addiction. Basically the study is just saying: Here is biologic proof for what you already know. That this is a biologically based disorder and the affected people are not just making a deliberate choice to behave this way.”
Dr. Wiznitzer said that a more interesting question is why this is a biological disorder.
“Is it something with which people were born with a tendency? Could it be something that somehow gets acquired? Does it need a gene-environment interaction in order to produce this? Does it occur after you’ve had some sort of injury? They didn’t ask these questions.”
In addition, he mentioned that some of these activation areas may be the same ones affected in certain mood disorders.
“People seem to have these mood munchies. One of the features of depression can be that they overeat. Or you hear of people with anxiety that also overeat. However, none of this was studied in this paper. In fact, they excluded anybody who had a mental disorder. It raises the question if this is the same mechanism for these disorders.”
Dr. Wiznitzer also noted that “in the old days when they did really aggressive surgeries,” certain brain sensors might get injured in a child when a tumor was being removed.
“After this type of injury, the children would turn into insatiable eaters. There was no off switch. So is this also one of the ultimate pathways?” he asked.
“In this study I think the people ate because there was some benefit. But I think others eat simply because they’re hungry and can’t get rid of that hunger. And I would argue that it’s worse for that group because you can’t treat it.”
The bottom line, he said, is that patients can exhibit the same behavior (overeating) yet have it come from different biologic causes.
“Even though it can’t answer all of them, this study brings up some very interesting questions,” concluded Dr. Wiznitzer.
The study was funded by a supplement grant from the National Institutes of Health Roadmap for Medical Research. The study authors and Dr. Wiznitzer have disclosed no relevant financial relationships.
Arch Gen Psychiatry.Published online April 4, 2011.
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