The politics of food addiction: Who wins, who 'loses'

ATLANTA – It’s too soon to disrupt current obesity treatment by declaring food addiction to be a clinical condition, according to Dr. Paul Fletcher.

"If we are to employ [the term] food addiction ... it needs a firm scientific basis," said Dr. Fletcher, who is the Bernard Wolfe Professor of Health Neuroscience in the department of psychiatry at University of Cambridge (England).

Organized medicine took the first step toward recognizing food addiction as a clinical diagnosis with the 2013 inclusion of binge eating disorder (BED) in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). That recognition has the potential to set the stage for an overhaul in delivery and funding of obesity treatment as well as how people with pathologic eating behaviors are viewed.

Obesogenic environment

For some, the answer to obesity and food addiction is to remove unhealthful foods from the environment. And to address "powerful environmental drives to consume them," Dr. Hisham Ziauddeen, a Wellcome Trust Fellow in Translational Medicine and Therapeutics at Cambridge, said in an interview.

In a separate presentation at a meeting, sponsored by the Obesity Society and the Society for the Study of Ingestive Behavior, Ashley Gearhardt, Ph.D., noted that researchers do not know whether food addiction exists. "The science is emerging." Foods high in fat and sugar, especially when aggressively marketed to children, are the chief culprits of the obesity epidemic, according to Dr. Gearhardt, a clinical psychologist at the University of Michigan, Ann Arbor.

"If scientific evidence identifies that certain foods are also capable of hijacking the brain in an addictive manner, it would likely be a landmark change that would support bold policy approaches that focus on improving the food environment," she has said (Biol. Psychiatry 2013;73:802-3).

Current research in the field is focused on the individual risk factors for compulsive eating, such as impulsivity or reward sensitivity, Dr. Gearhardt said. However, the lack of addictive behaviors associated with "minimally processed foods that are relatively low in sugar and fat, such as apples or chicken breasts," means research now needs to determine if there is something about the food or behavior "that leads to compulsive problematic use," she said in an interview.

"Individual approaches may be helpful in developing clinical interventions but will touch the lives of far fewer people than will policy changes that affect entire populations," she said.

Dr. Gearhardt and her associates sought to link obesity to addictive patterning in the brain through the combined use of functional neuroimaging (fMRI) and scores on the Yale Food Addiction Scale (YFAS), which applies substance-dependence criteria in the DSM-IV-TR as a type of metric for addictive eating behaviors.

The investigators used fMRI maps of participants’ brain activation when they were given food cues of either a tasteless substance or a chocolate milkshake high in fat and sugar. These images were then compared with the participants’ scores from the YFAS. The group was a mixture of both lean and obese women (Arch. Gen. Psychiatry. 2011;68:808-16).

The researchers found that when presented with a chocolate milkshake, those with higher YFAS scores, regardless of body mass index, experienced "significantly greater activation" in brain regions associated with dopaminergic release, including the anterior cingulate cortex. Those with the highest YFAS scores experienced a significant increase in activity of the dorsolateral prefrontal cortex.

‘Elegant experiments’

While fMRI research into the neurobiologic response to food has "generated some very elegant experiments," according to Dr. Fletcher, he is concerned that food addiction proponents have neglected to see these data in a larger context. "The literature is hugely inconsistent, and ignoring this fact may be inconvenient ... but if we continue to do so, it will come back to slap us in the face."

Because neuroimages "are often ambiguous, unless they are constrained by a specific hypothesis, it becomes more like reading tarot cards than interpreting scientific data," he said. "There is a dangerous tendency for people to have a particular perspective and then, no matter what the fMRI data show, to interpret them according to the perspective with which they started out."

And while this free hand with data interpretation happens generally, Dr. Fletcher said he has been "particularly struck" by its occurrence in the food addiction field. "There seem to be very few constraints on interpretation of the regional activation," he said, noting that whether researchers are looking at obesity, binge-eating, or anyone assumed to have a food addition. "Inevitably, [the researchers] find differences in neural activation in such groups but the interpretations of those activations are often post hoc and heavily biased by what the researchers believed in the first place."

As an example, he cited how activity in the anterior cingulate cortex in overweight people given food cues may be interpreted as a sign of craving. "But this is an unjustified inference because we do not know what the anterior cingulate cortex does and it far more frequently related to other processes than to craving."

Dr. Fletcher and his colleagues’ alarm over this "oversimplification of data" prompted a polite, but impassioned, back and forth with Dr. Gearhardt and her associates, published in Nature Reviews Neuroscience (2012;13:279-86 [doi:10.1038/nrn3212]); (2012;13:514 [doi:10.1038/nrn3212-c1]); (2012;13:514 [doi:10.1038/nrn3212-c2]).

In the first of these editorials, Dr. Fletcher and his coauthors wrote that "the messages now emerging from the neuroscientific research community may therefore have an unprecedented impact on policy development," and in another, urged the adoption of "a more detailed consideration" of how to explore food addiction, particularly since cognitive neuroscience is already moving the field beyond ideas based "purely on clinical overlap" and the model of addiction as delineated in the DSM-IV-TR.

Obesity subsets

"Dr. Fletcher and I agree that the concept of ‘food addiction’ is still an open question," Dr. Gearhardt said in an interview. "My group believes that there is evidence building that suggests it is plausible that an addictive process contributes to problematic eating in some circumstances, especially for eaters who exhibit behavioral phenotypes."

Binge eating, emotional eating, and other pathologies surrounding attitudes toward food also were noted in participants with high YFAS scores in Dr. Gearhardt’s study. "We see evidence of addictive-like processes contributing to problematic eating even for individuals who do not meet the criteria for BED," she said.

Dr. Fletcher noted that "there is a clear degree of clinical overlap between obesity and binge eating, particularly binge eating disorder and drug addiction." Specifically, tolerance, withdrawal, persistent desire for food, eating more than intended, and the diminishment of social engagement in exchange for more time spent acquiring and ingesting food all parallel drug addiction. "However, we don’t know what the overlap is," said Dr. Fletcher. "Is it sugar? Is it fat? Is it a combination? We really don’t know yet."

Populations vs. individuals

"If certain foods are addictive, this may partially explain the difficulty people experience in achieving sustainable weight loss," according to Dr. Gearhardt in commenting on the fMRI study results. "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."

Dr. Gearhardt speculated that a focus on specific food ingredients being at the root of addiction-linked obesity may spur activism by manufacturers. "The food industry will likely use any inconsistency in the food addiction literature to plant doubt, attack scientists’ credibility, or fund negative studies," they wrote.

By focusing on how detrimental the food environment has become as a result of "heavily marketed foods that interact with the brain in harmful ways," the public may be more likely to support restrictive policies such as "taxing addictive foods, limiting marketing of these foods to children, and enacting zoning laws that limit the number of vendors selling such foods" among other measures, she wrote.

Dr. Fletcher acknowledged that there is likely a legitimate "battle to be joined" against marketers of junk food and other agents contributing to a deleterious food environment, but attacking the problem at the societal level without consideration of the potential impact on the individual will ultimately backfire. "We must be very careful about how we line up our troops," he said.

"Changing behavior at a population level, which indubitably is required, is not going to be easy," said Dr. Ziauddeen. "As well as the resistance of those with vested interests, such changes will be considered widely unacceptable if they are perceived to entail a loss of liberty."

Although Dr. Fletcher and Dr. Ziauddeen agree a lack of willpower and moral frailty are antiquated notions of why people become obese, assuming that diagnosing people as food addicts will protect them, either from stigmatization or any unforeseen effects of policy changes, is short-sighted.

"Based on our experience with drug addictions over the centuries, it is hard to think that food addiction will not come with some stigma and the consequences thereof," he said.

And Dr. Ziauddeen agreed that, "If the science is shaky and hard to defend, it will be ripped apart." Beyond it possibly being "indefensible" in the face of the opposition from processed food manufacturers, thus setting the field back on its heels, there is the danger of a loss of personal liberty that results, not for the sake of the greater good, but solely from policies based on shoddy science.

"The removal of choice is less threatening if it is done to protect against a situation in which the individual has no real choice anyway, as is the case with addictive substances," said Dr. Ziauddeen. "In short, if there is an addictive agent in some foods, then policy change and legislation can be seen as protective rather than restrictive." This is only possible however, he said, if there is "clear, consistent evidence that there is indeed an addictive substance in food."

And yet, regarding a connection between obesity and food addiction, "the most striking finding is complete inconsistency," said Dr. Fletcher. "I would like to see the same sorts of changes that those supporting food addiction would like, but I do not think that we are going to succeed by using a poorly specified concept with little real evidence to back it up."

Dopamine response not reliable measure

"Food addiction may well exist, [but] even then, it may only explain a tiny fraction of obesity and overeating," according to Dr. Fletcher. "Perhaps the major problem is our general limitations in our often dopaminergically centered views of what constitutes addiction."

A full understanding of the brain’s pathophysiology is still under development, he said. But in addition to classic behavioral manifestations, such as persistent use of a substance, accepted components of addiction include reduced dopamine-receptor density in the ventral striatum and a flip in the neurocircuitry for decision making from the ventral to the dorsal striatum.

Otherwise, he said, conclusive statements about the neurobiology of addiction are suspect. "When we run a functional neuroimaging experiment, we are looking at many different brain regions and, for pretty much all of these, there is a fairly dense ambiguity about what processes they carry out."

In addition, said Dr. Fletcher, although several researchers have tried to replicate one particular study showing that that showed those with severe obesity had reduced raclopride, an indication their dopamine reception was suppressed, the various findings have been inconsistent, thus, said Dr. Fletcher, "there is no proof that there is reduced dopamine in obesity" (Lancet 2001;357:354-7).

As the field of addiction research advances, there will be a shift in the viewpoint that dopamine is the "end all and be all," in part because there will be a deeper understanding of individual variability to different substances that lead to different forms of eating pathologies, he said. "We need to entertain the notion that no single characteristic will define the nature of reward-processing in obesity and that there may be many routes to positive calorie balance."

Longitudinal studies of individual variability to certain foods also could help better determine the impact of certain foods on the brain, he said.

Winners and ‘losers’

"In terms of those who stand to gain from the acceptance of food addiction," said Dr. Fletcher, "At first glance, this would seem to be the people who offer treatments for food addiction and the people who might make some money by suing [processed food] companies."

Yet, for Dr. Gearhardt, if food addiction is proved, and a direct line can be drawn between the food industry’s intentional manipulation of ingredients to profit from this "brain hijacking," Dr. Gearhardt said, "This brings up the question of industry culpability and the ethics of aggressively marketing it to children."

Dr. Gearhardt also believes the possibility of a clinical food addiction diagnosis for those who struggle with pathological eating might "encourage more people ... to receive professional help rather than beat themselves up for not being able to stick to diet after diet on their own."

Conversely, Dr. Ziauddeen noted what while a food addiction diagnosis may offer someone consolation and motivation to seek help, "What if the person is subject to restrictions or treatments based on the diagnosis?" Specifically, he cited ineligibility for bariatric surgery or less clout in the eyes of the court for child custody. "This does not require a stretch of the imagination," he said. "If you have a diagnosis of alcohol dependence, it influences your chances of receiving a liver transplant. If you have a diagnosis of drug or alcohol addiction, it impacts social care decisions made about your children."

Accepting food addiction as real will affect not only those given the diagnosis, but also the so-called "unaffected" public, said Dr. Fletcher. "If food ‘X’ is addictive, to what extent should it be controlled?" He also suggested that health care provision would experience overhaul: "What will be the effect of diverting funding to food addiction treatment from other obesity-related treatments?"

Food addiction "may help us think of novel and hopefully more effective strategies for treating eating-related concerns," said Dr. Gearhardt.

Regardless, Dr. Fletcher warned that because obesity is multifactorial, and includes molecular, metabolic, behavioral, societal and environmental elements, we should not rush to accept "simplistic" answers, or force things to fit where they actually might not. "The thing I think we need to stop right now is this selective citing because we like the narrative."

Dr. Fletcher, Dr. Ziauddeen, and Dr. Gearhardt had no relevant disclosures.

[email protected]

ATLANTA – It’s too soon to disrupt current obesity treatment by declaring food addiction to be a clinical condition, according to Dr. Paul Fletcher.

"If we are to employ [the term] food addiction ... it needs a firm scientific basis," said Dr. Fletcher, who is the Bernard Wolfe Professor of Health Neuroscience in the department of psychiatry at University of Cambridge (England).

Organized medicine took the first step toward recognizing food addiction as a clinical diagnosis with the 2013 inclusion of binge eating disorder (BED) in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). That recognition has the potential to set the stage for an overhaul in delivery and funding of obesity treatment as well as how people with pathologic eating behaviors are viewed.

Obesogenic environment

For some, the answer to obesity and food addiction is to remove unhealthful foods from the environment. And to address "powerful environmental drives to consume them," Dr. Hisham Ziauddeen, a Wellcome Trust Fellow in Translational Medicine and Therapeutics at Cambridge, said in an interview.

In a separate presentation at a meeting, sponsored by the Obesity Society and the Society for the Study of Ingestive Behavior, Ashley Gearhardt, Ph.D., noted that researchers do not know whether food addiction exists. "The science is emerging." Foods high in fat and sugar, especially when aggressively marketed to children, are the chief culprits of the obesity epidemic, according to Dr. Gearhardt, a clinical psychologist at the University of Michigan, Ann Arbor.

"If scientific evidence identifies that certain foods are also capable of hijacking the brain in an addictive manner, it would likely be a landmark change that would support bold policy approaches that focus on improving the food environment," she has said (Biol. Psychiatry 2013;73:802-3).

Current research in the field is focused on the individual risk factors for compulsive eating, such as impulsivity or reward sensitivity, Dr. Gearhardt said. However, the lack of addictive behaviors associated with "minimally processed foods that are relatively low in sugar and fat, such as apples or chicken breasts," means research now needs to determine if there is something about the food or behavior "that leads to compulsive problematic use," she said in an interview.

"Individual approaches may be helpful in developing clinical interventions but will touch the lives of far fewer people than will policy changes that affect entire populations," she said.

Dr. Gearhardt and her associates sought to link obesity to addictive patterning in the brain through the combined use of functional neuroimaging (fMRI) and scores on the Yale Food Addiction Scale (YFAS), which applies substance-dependence criteria in the DSM-IV-TR as a type of metric for addictive eating behaviors.

The investigators used fMRI maps of participants’ brain activation when they were given food cues of either a tasteless substance or a chocolate milkshake high in fat and sugar. These images were then compared with the participants’ scores from the YFAS. The group was a mixture of both lean and obese women (Arch. Gen. Psychiatry. 2011;68:808-16).

The researchers found that when presented with a chocolate milkshake, those with higher YFAS scores, regardless of body mass index, experienced "significantly greater activation" in brain regions associated with dopaminergic release, including the anterior cingulate cortex. Those with the highest YFAS scores experienced a significant increase in activity of the dorsolateral prefrontal cortex.

‘Elegant experiments’

While fMRI research into the neurobiologic response to food has "generated some very elegant experiments," according to Dr. Fletcher, he is concerned that food addiction proponents have neglected to see these data in a larger context. "The literature is hugely inconsistent, and ignoring this fact may be inconvenient ... but if we continue to do so, it will come back to slap us in the face."

Because neuroimages "are often ambiguous, unless they are constrained by a specific hypothesis, it becomes more like reading tarot cards than interpreting scientific data," he said. "There is a dangerous tendency for people to have a particular perspective and then, no matter what the fMRI data show, to interpret them according to the perspective with which they started out."

And while this free hand with data interpretation happens generally, Dr. Fletcher said he has been "particularly struck" by its occurrence in the food addiction field. "There seem to be very few constraints on interpretation of the regional activation," he said, noting that whether researchers are looking at obesity, binge-eating, or anyone assumed to have a food addition. "Inevitably, [the researchers] find differences in neural activation in such groups but the interpretations of those activations are often post hoc and heavily biased by what the researchers believed in the first place."

As an example, he cited how activity in the anterior cingulate cortex in overweight people given food cues may be interpreted as a sign of craving. "But this is an unjustified inference because we do not know what the anterior cingulate cortex does and it far more frequently related to other processes than to craving."

Dr. Fletcher and his colleagues’ alarm over this "oversimplification of data" prompted a polite, but impassioned, back and forth with Dr. Gearhardt and her associates, published in Nature Reviews Neuroscience (2012;13:279-86 [doi:10.1038/nrn3212]); (2012;13:514 [doi:10.1038/nrn3212-c1]); (2012;13:514 [doi:10.1038/nrn3212-c2]).

In the first of these editorials, Dr. Fletcher and his coauthors wrote that "the messages now emerging from the neuroscientific research community may therefore have an unprecedented impact on policy development," and in another, urged the adoption of "a more detailed consideration" of how to explore food addiction, particularly since cognitive neuroscience is already moving the field beyond ideas based "purely on clinical overlap" and the model of addiction as delineated in the DSM-IV-TR.

Obesity subsets

"Dr. Fletcher and I agree that the concept of ‘food addiction’ is still an open question," Dr. Gearhardt said in an interview. "My group believes that there is evidence building that suggests it is plausible that an addictive process contributes to problematic eating in some circumstances, especially for eaters who exhibit behavioral phenotypes."

Binge eating, emotional eating, and other pathologies surrounding attitudes toward food also were noted in participants with high YFAS scores in Dr. Gearhardt’s study. "We see evidence of addictive-like processes contributing to problematic eating even for individuals who do not meet the criteria for BED," she said.

Dr. Fletcher noted that "there is a clear degree of clinical overlap between obesity and binge eating, particularly binge eating disorder and drug addiction." Specifically, tolerance, withdrawal, persistent desire for food, eating more than intended, and the diminishment of social engagement in exchange for more time spent acquiring and ingesting food all parallel drug addiction. "However, we don’t know what the overlap is," said Dr. Fletcher. "Is it sugar? Is it fat? Is it a combination? We really don’t know yet."

Populations vs. individuals

"If certain foods are addictive, this may partially explain the difficulty people experience in achieving sustainable weight loss," according to Dr. Gearhardt in commenting on the fMRI study results. "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."

Dr. Gearhardt speculated that a focus on specific food ingredients being at the root of addiction-linked obesity may spur activism by manufacturers. "The food industry will likely use any inconsistency in the food addiction literature to plant doubt, attack scientists’ credibility, or fund negative studies," they wrote.

By focusing on how detrimental the food environment has become as a result of "heavily marketed foods that interact with the brain in harmful ways," the public may be more likely to support restrictive policies such as "taxing addictive foods, limiting marketing of these foods to children, and enacting zoning laws that limit the number of vendors selling such foods" among other measures, she wrote.

Dr. Fletcher acknowledged that there is likely a legitimate "battle to be joined" against marketers of junk food and other agents contributing to a deleterious food environment, but attacking the problem at the societal level without consideration of the potential impact on the individual will ultimately backfire. "We must be very careful about how we line up our troops," he said.

"Changing behavior at a population level, which indubitably is required, is not going to be easy," said Dr. Ziauddeen. "As well as the resistance of those with vested interests, such changes will be considered widely unacceptable if they are perceived to entail a loss of liberty."

Although Dr. Fletcher and Dr. Ziauddeen agree a lack of willpower and moral frailty are antiquated notions of why people become obese, assuming that diagnosing people as food addicts will protect them, either from stigmatization or any unforeseen effects of policy changes, is short-sighted.

"Based on our experience with drug addictions over the centuries, it is hard to think that food addiction will not come with some stigma and the consequences thereof," he said.

And Dr. Ziauddeen agreed that, "If the science is shaky and hard to defend, it will be ripped apart." Beyond it possibly being "indefensible" in the face of the opposition from processed food manufacturers, thus setting the field back on its heels, there is the danger of a loss of personal liberty that results, not for the sake of the greater good, but solely from policies based on shoddy science.

"The removal of choice is less threatening if it is done to protect against a situation in which the individual has no real choice anyway, as is the case with addictive substances," said Dr. Ziauddeen. "In short, if there is an addictive agent in some foods, then policy change and legislation can be seen as protective rather than restrictive." This is only possible however, he said, if there is "clear, consistent evidence that there is indeed an addictive substance in food."

And yet, regarding a connection between obesity and food addiction, "the most striking finding is complete inconsistency," said Dr. Fletcher. "I would like to see the same sorts of changes that those supporting food addiction would like, but I do not think that we are going to succeed by using a poorly specified concept with little real evidence to back it up."

Dopamine response not reliable measure

"Food addiction may well exist, [but] even then, it may only explain a tiny fraction of obesity and overeating," according to Dr. Fletcher. "Perhaps the major problem is our general limitations in our often dopaminergically centered views of what constitutes addiction."

A full understanding of the brain’s pathophysiology is still under development, he said. But in addition to classic behavioral manifestations, such as persistent use of a substance, accepted components of addiction include reduced dopamine-receptor density in the ventral striatum and a flip in the neurocircuitry for decision making from the ventral to the dorsal striatum.

Otherwise, he said, conclusive statements about the neurobiology of addiction are suspect. "When we run a functional neuroimaging experiment, we are looking at many different brain regions and, for pretty much all of these, there is a fairly dense ambiguity about what processes they carry out."

In addition, said Dr. Fletcher, although several researchers have tried to replicate one particular study showing that that showed those with severe obesity had reduced raclopride, an indication their dopamine reception was suppressed, the various findings have been inconsistent, thus, said Dr. Fletcher, "there is no proof that there is reduced dopamine in obesity" (Lancet 2001;357:354-7).

As the field of addiction research advances, there will be a shift in the viewpoint that dopamine is the "end all and be all," in part because there will be a deeper understanding of individual variability to different substances that lead to different forms of eating pathologies, he said. "We need to entertain the notion that no single characteristic will define the nature of reward-processing in obesity and that there may be many routes to positive calorie balance."

Longitudinal studies of individual variability to certain foods also could help better determine the impact of certain foods on the brain, he said.

Winners and ‘losers’

"In terms of those who stand to gain from the acceptance of food addiction," said Dr. Fletcher, "At first glance, this would seem to be the people who offer treatments for food addiction and the people who might make some money by suing [processed food] companies."

Yet, for Dr. Gearhardt, if food addiction is proved, and a direct line can be drawn between the food industry’s intentional manipulation of ingredients to profit from this "brain hijacking," Dr. Gearhardt said, "This brings up the question of industry culpability and the ethics of aggressively marketing it to children."

Dr. Gearhardt also believes the possibility of a clinical food addiction diagnosis for those who struggle with pathological eating might "encourage more people ... to receive professional help rather than beat themselves up for not being able to stick to diet after diet on their own."

Conversely, Dr. Ziauddeen noted what while a food addiction diagnosis may offer someone consolation and motivation to seek help, "What if the person is subject to restrictions or treatments based on the diagnosis?" Specifically, he cited ineligibility for bariatric surgery or less clout in the eyes of the court for child custody. "This does not require a stretch of the imagination," he said. "If you have a diagnosis of alcohol dependence, it influences your chances of receiving a liver transplant. If you have a diagnosis of drug or alcohol addiction, it impacts social care decisions made about your children."

Accepting food addiction as real will affect not only those given the diagnosis, but also the so-called "unaffected" public, said Dr. Fletcher. "If food ‘X’ is addictive, to what extent should it be controlled?" He also suggested that health care provision would experience overhaul: "What will be the effect of diverting funding to food addiction treatment from other obesity-related treatments?"

Food addiction "may help us think of novel and hopefully more effective strategies for treating eating-related concerns," said Dr. Gearhardt.

Regardless, Dr. Fletcher warned that because obesity is multifactorial, and includes molecular, metabolic, behavioral, societal and environmental elements, we should not rush to accept "simplistic" answers, or force things to fit where they actually might not. "The thing I think we need to stop right now is this selective citing because we like the narrative."

Dr. Fletcher, Dr. Ziauddeen, and Dr. Gearhardt had no relevant disclosures.

[email protected]

ATLANTA – It’s too soon to disrupt current obesity treatment by declaring food addiction to be a clinical condition, according to Dr. Paul Fletcher.

"If we are to employ [the term] food addiction ... it needs a firm scientific basis," said Dr. Fletcher, who is the Bernard Wolfe Professor of Health Neuroscience in the department of psychiatry at University of Cambridge (England).

Organized medicine took the first step toward recognizing food addiction as a clinical diagnosis with the 2013 inclusion of binge eating disorder (BED) in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). That recognition has the potential to set the stage for an overhaul in delivery and funding of obesity treatment as well as how people with pathologic eating behaviors are viewed.

Obesogenic environment

For some, the answer to obesity and food addiction is to remove unhealthful foods from the environment. And to address "powerful environmental drives to consume them," Dr. Hisham Ziauddeen, a Wellcome Trust Fellow in Translational Medicine and Therapeutics at Cambridge, said in an interview.

In a separate presentation at a meeting, sponsored by the Obesity Society and the Society for the Study of Ingestive Behavior, Ashley Gearhardt, Ph.D., noted that researchers do not know whether food addiction exists. "The science is emerging." Foods high in fat and sugar, especially when aggressively marketed to children, are the chief culprits of the obesity epidemic, according to Dr. Gearhardt, a clinical psychologist at the University of Michigan, Ann Arbor.

"If scientific evidence identifies that certain foods are also capable of hijacking the brain in an addictive manner, it would likely be a landmark change that would support bold policy approaches that focus on improving the food environment," she has said (Biol. Psychiatry 2013;73:802-3).

Current research in the field is focused on the individual risk factors for compulsive eating, such as impulsivity or reward sensitivity, Dr. Gearhardt said. However, the lack of addictive behaviors associated with "minimally processed foods that are relatively low in sugar and fat, such as apples or chicken breasts," means research now needs to determine if there is something about the food or behavior "that leads to compulsive problematic use," she said in an interview.

"Individual approaches may be helpful in developing clinical interventions but will touch the lives of far fewer people than will policy changes that affect entire populations," she said.

Dr. Gearhardt and her associates sought to link obesity to addictive patterning in the brain through the combined use of functional neuroimaging (fMRI) and scores on the Yale Food Addiction Scale (YFAS), which applies substance-dependence criteria in the DSM-IV-TR as a type of metric for addictive eating behaviors.

The investigators used fMRI maps of participants’ brain activation when they were given food cues of either a tasteless substance or a chocolate milkshake high in fat and sugar. These images were then compared with the participants’ scores from the YFAS. The group was a mixture of both lean and obese women (Arch. Gen. Psychiatry. 2011;68:808-16).

The researchers found that when presented with a chocolate milkshake, those with higher YFAS scores, regardless of body mass index, experienced "significantly greater activation" in brain regions associated with dopaminergic release, including the anterior cingulate cortex. Those with the highest YFAS scores experienced a significant increase in activity of the dorsolateral prefrontal cortex.

‘Elegant experiments’

While fMRI research into the neurobiologic response to food has "generated some very elegant experiments," according to Dr. Fletcher, he is concerned that food addiction proponents have neglected to see these data in a larger context. "The literature is hugely inconsistent, and ignoring this fact may be inconvenient ... but if we continue to do so, it will come back to slap us in the face."

Because neuroimages "are often ambiguous, unless they are constrained by a specific hypothesis, it becomes more like reading tarot cards than interpreting scientific data," he said. "There is a dangerous tendency for people to have a particular perspective and then, no matter what the fMRI data show, to interpret them according to the perspective with which they started out."

And while this free hand with data interpretation happens generally, Dr. Fletcher said he has been "particularly struck" by its occurrence in the food addiction field. "There seem to be very few constraints on interpretation of the regional activation," he said, noting that whether researchers are looking at obesity, binge-eating, or anyone assumed to have a food addition. "Inevitably, [the researchers] find differences in neural activation in such groups but the interpretations of those activations are often post hoc and heavily biased by what the researchers believed in the first place."

As an example, he cited how activity in the anterior cingulate cortex in overweight people given food cues may be interpreted as a sign of craving. "But this is an unjustified inference because we do not know what the anterior cingulate cortex does and it far more frequently related to other processes than to craving."

Dr. Fletcher and his colleagues’ alarm over this "oversimplification of data" prompted a polite, but impassioned, back and forth with Dr. Gearhardt and her associates, published in Nature Reviews Neuroscience (2012;13:279-86 [doi:10.1038/nrn3212]); (2012;13:514 [doi:10.1038/nrn3212-c1]); (2012;13:514 [doi:10.1038/nrn3212-c2]).

In the first of these editorials, Dr. Fletcher and his coauthors wrote that "the messages now emerging from the neuroscientific research community may therefore have an unprecedented impact on policy development," and in another, urged the adoption of "a more detailed consideration" of how to explore food addiction, particularly since cognitive neuroscience is already moving the field beyond ideas based "purely on clinical overlap" and the model of addiction as delineated in the DSM-IV-TR.

Obesity subsets

"Dr. Fletcher and I agree that the concept of ‘food addiction’ is still an open question," Dr. Gearhardt said in an interview. "My group believes that there is evidence building that suggests it is plausible that an addictive process contributes to problematic eating in some circumstances, especially for eaters who exhibit behavioral phenotypes."

Binge eating, emotional eating, and other pathologies surrounding attitudes toward food also were noted in participants with high YFAS scores in Dr. Gearhardt’s study. "We see evidence of addictive-like processes contributing to problematic eating even for individuals who do not meet the criteria for BED," she said.

Dr. Fletcher noted that "there is a clear degree of clinical overlap between obesity and binge eating, particularly binge eating disorder and drug addiction." Specifically, tolerance, withdrawal, persistent desire for food, eating more than intended, and the diminishment of social engagement in exchange for more time spent acquiring and ingesting food all parallel drug addiction. "However, we don’t know what the overlap is," said Dr. Fletcher. "Is it sugar? Is it fat? Is it a combination? We really don’t know yet."

Populations vs. individuals

"If certain foods are addictive, this may partially explain the difficulty people experience in achieving sustainable weight loss," according to Dr. Gearhardt in commenting on the fMRI study results. "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."

Dr. Gearhardt speculated that a focus on specific food ingredients being at the root of addiction-linked obesity may spur activism by manufacturers. "The food industry will likely use any inconsistency in the food addiction literature to plant doubt, attack scientists’ credibility, or fund negative studies," they wrote.

By focusing on how detrimental the food environment has become as a result of "heavily marketed foods that interact with the brain in harmful ways," the public may be more likely to support restrictive policies such as "taxing addictive foods, limiting marketing of these foods to children, and enacting zoning laws that limit the number of vendors selling such foods" among other measures, she wrote.

Dr. Fletcher acknowledged that there is likely a legitimate "battle to be joined" against marketers of junk food and other agents contributing to a deleterious food environment, but attacking the problem at the societal level without consideration of the potential impact on the individual will ultimately backfire. "We must be very careful about how we line up our troops," he said.

"Changing behavior at a population level, which indubitably is required, is not going to be easy," said Dr. Ziauddeen. "As well as the resistance of those with vested interests, such changes will be considered widely unacceptable if they are perceived to entail a loss of liberty."

Although Dr. Fletcher and Dr. Ziauddeen agree a lack of willpower and moral frailty are antiquated notions of why people become obese, assuming that diagnosing people as food addicts will protect them, either from stigmatization or any unforeseen effects of policy changes, is short-sighted.

"Based on our experience with drug addictions over the centuries, it is hard to think that food addiction will not come with some stigma and the consequences thereof," he said.

And Dr. Ziauddeen agreed that, "If the science is shaky and hard to defend, it will be ripped apart." Beyond it possibly being "indefensible" in the face of the opposition from processed food manufacturers, thus setting the field back on its heels, there is the danger of a loss of personal liberty that results, not for the sake of the greater good, but solely from policies based on shoddy science.

"The removal of choice is less threatening if it is done to protect against a situation in which the individual has no real choice anyway, as is the case with addictive substances," said Dr. Ziauddeen. "In short, if there is an addictive agent in some foods, then policy change and legislation can be seen as protective rather than restrictive." This is only possible however, he said, if there is "clear, consistent evidence that there is indeed an addictive substance in food."

And yet, regarding a connection between obesity and food addiction, "the most striking finding is complete inconsistency," said Dr. Fletcher. "I would like to see the same sorts of changes that those supporting food addiction would like, but I do not think that we are going to succeed by using a poorly specified concept with little real evidence to back it up."

Dopamine response not reliable measure

"Food addiction may well exist, [but] even then, it may only explain a tiny fraction of obesity and overeating," according to Dr. Fletcher. "Perhaps the major problem is our general limitations in our often dopaminergically centered views of what constitutes addiction."

A full understanding of the brain’s pathophysiology is still under development, he said. But in addition to classic behavioral manifestations, such as persistent use of a substance, accepted components of addiction include reduced dopamine-receptor density in the ventral striatum and a flip in the neurocircuitry for decision making from the ventral to the dorsal striatum.

Otherwise, he said, conclusive statements about the neurobiology of addiction are suspect. "When we run a functional neuroimaging experiment, we are looking at many different brain regions and, for pretty much all of these, there is a fairly dense ambiguity about what processes they carry out."

In addition, said Dr. Fletcher, although several researchers have tried to replicate one particular study showing that that showed those with severe obesity had reduced raclopride, an indication their dopamine reception was suppressed, the various findings have been inconsistent, thus, said Dr. Fletcher, "there is no proof that there is reduced dopamine in obesity" (Lancet 2001;357:354-7).

As the field of addiction research advances, there will be a shift in the viewpoint that dopamine is the "end all and be all," in part because there will be a deeper understanding of individual variability to different substances that lead to different forms of eating pathologies, he said. "We need to entertain the notion that no single characteristic will define the nature of reward-processing in obesity and that there may be many routes to positive calorie balance."

Longitudinal studies of individual variability to certain foods also could help better determine the impact of certain foods on the brain, he said.

Winners and ‘losers’

"In terms of those who stand to gain from the acceptance of food addiction," said Dr. Fletcher, "At first glance, this would seem to be the people who offer treatments for food addiction and the people who might make some money by suing [processed food] companies."

Yet, for Dr. Gearhardt, if food addiction is proved, and a direct line can be drawn between the food industry’s intentional manipulation of ingredients to profit from this "brain hijacking," Dr. Gearhardt said, "This brings up the question of industry culpability and the ethics of aggressively marketing it to children."

Dr. Gearhardt also believes the possibility of a clinical food addiction diagnosis for those who struggle with pathological eating might "encourage more people ... to receive professional help rather than beat themselves up for not being able to stick to diet after diet on their own."

Conversely, Dr. Ziauddeen noted what while a food addiction diagnosis may offer someone consolation and motivation to seek help, "What if the person is subject to restrictions or treatments based on the diagnosis?" Specifically, he cited ineligibility for bariatric surgery or less clout in the eyes of the court for child custody. "This does not require a stretch of the imagination," he said. "If you have a diagnosis of alcohol dependence, it influences your chances of receiving a liver transplant. If you have a diagnosis of drug or alcohol addiction, it impacts social care decisions made about your children."

Accepting food addiction as real will affect not only those given the diagnosis, but also the so-called "unaffected" public, said Dr. Fletcher. "If food ‘X’ is addictive, to what extent should it be controlled?" He also suggested that health care provision would experience overhaul: "What will be the effect of diverting funding to food addiction treatment from other obesity-related treatments?"

Food addiction "may help us think of novel and hopefully more effective strategies for treating eating-related concerns," said Dr. Gearhardt.

Regardless, Dr. Fletcher warned that because obesity is multifactorial, and includes molecular, metabolic, behavioral, societal and environmental elements, we should not rush to accept "simplistic" answers, or force things to fit where they actually might not. "The thing I think we need to stop right now is this selective citing because we like the narrative."

Dr. Fletcher, Dr. Ziauddeen, and Dr. Gearhardt had no relevant disclosures.

[email protected]