Are We Addicted to Food? -- Del Parigi et al. 11 (4): 493 -- Obesity
Are We Addicted to Food?
Angelo Del Parigi*, Kewei Chen, Arline D. Salbe*, Eric M. Reiman and P. Antonio Tataranni*
* Clinical Diabetes and Nutrition Section, National Institutes of Health, Phoenix, Arizona; and
PET Research Center, Good Samaritan Hospital, Phoenix, Arizona.
Address correspondence to Angelo Del Parigi, MD, Clinical Diabetes and Nutrition Section, National Institutes of Health, 4212 N. 16th St., Rm. 541, Phoenix, AZ 85016. E-mail: adelpari@mail.nih.gov
Introduction
As the battle of the bulge seems headed toward becoming the "culture war of the new century," with state legislatures discussing and/or passing bills to ban "junk food" from schools and trial lawyers gearing up to file lawsuits against the food industry, much as they did against the tobacco industry (1) (2) , it is very likely that the scientific community will come under increasing pressure to answer the question of why we eat so much.
Rare forms of obesity caused by defects of the energy homeostasis regulatory mechanisms operating in the subconscious brain have been described in animals and humans (3) . However, eating is as much a means of achieving energy balance as it is a form of pleasure and reward. This makes the drive to eat one of the most powerful urges of animal and human behavior.
Reward, Addiction, and Food
The behavioral outcome of a reward is in making subjects "come back for more" by conditioning the approach and consumption activity to the hedonic feelings derived from the anticipation and attainment of the desired object (4) .
The parallel between drug dependence, which is the condition originally defined as addiction, and overeating, which leads to obesity, may not seem immediately apparent. Addiction is a chronically relapsing disorder characterized by compulsion to seek and take the drug; loss of control in limiting intake of the drug; and onset of a negative emotional state (e.g., anxiety, irritability) when access to the drug is prevented (i.e., dependence) (5) . In addicted drug users, craving is elicited by exposure to drug-related cues, which may trigger a relapse. A similar behavior characterizes the craving for food in overeaters (6) . It is known that eating disorders tend to cluster with drug and alcohol abuse in individuals and families (6) , and common neural circuits are thought to underlie food and drug rewards, including opioid (7) (8) (9) , serotoninergic (8) (9) , and dopaminergic pathways (8) (9) (10) . It has been proposed that the dopaminergic brain circuitry underlying addictions originally developed to subserve eating behavior (11) . However, whereas food is the most common and natural source of pleasure in everyday life and the neurophysiology of reward in humans has been extensively studied in the context of drug abuse (12) , little is known about how the human brain specifically processes food reward.
Role of Dopamine in Modulating Eating Behavior
[...]
However, the brain’s response to food reward is not likely to be confined to the striatum. Consistent with lesion studies in animals (9) , neuroimaging studies in humans have provided converging evidence that the central processing of food reward consistently overlaps with the sensory and visceral responses to ingestion of food in the insula, orbitofrontal cortex, and anteromedial temporal lobe (30) , areas that receive dopaminergic afferents through the mesolimbic and mesocortical pathways. Interestingly, in some of these areas, we observed a larger decrease of activity in obese compared with lean men (p < 0.001) (29) . Taken together, this evidence suggests that the cortical processing of food sensory cues participates in the motivational aspects of eating behavior. How this cortical processing may be affected by cognitive stimuli such as food advertisements in different communication media and how it may reinforce eating habits remain to be established.
Conclusions
Do we have enough new evidence from neurofunctional and other studies to begin to suspect that human obesity is predominantly an addictive disorder characterized by compulsive eating? We cannot say for sure, as yet. Some critical steps needed to further our understanding include establishing [as preliminary data seem to suggest (31) ] whether dopamine is released in response to food ingestion in humans (as it is in animals) and establishing the pathophysiological meaning of selective neurophysiological differences between obese and lean individuals. This may be accomplished by studying the brain and its dopaminergic pathways in individuals at high risk for the disease before they gain weight and become frankly obese. Nevertheless, we contend that more research on the role of the brain in the etiology of weight gain may help us understand if the current epidemic of obesity, which we are helplessly watching spread around the world, is a global case of food addiction.
Are We Addicted to Food?
Angelo Del Parigi*, Kewei Chen, Arline D. Salbe*, Eric M. Reiman and P. Antonio Tataranni*
* Clinical Diabetes and Nutrition Section, National Institutes of Health, Phoenix, Arizona; and
PET Research Center, Good Samaritan Hospital, Phoenix, Arizona.
Address correspondence to Angelo Del Parigi, MD, Clinical Diabetes and Nutrition Section, National Institutes of Health, 4212 N. 16th St., Rm. 541, Phoenix, AZ 85016. E-mail: adelpari@mail.nih.gov
Introduction
As the battle of the bulge seems headed toward becoming the "culture war of the new century," with state legislatures discussing and/or passing bills to ban "junk food" from schools and trial lawyers gearing up to file lawsuits against the food industry, much as they did against the tobacco industry (1) (2) , it is very likely that the scientific community will come under increasing pressure to answer the question of why we eat so much.
Rare forms of obesity caused by defects of the energy homeostasis regulatory mechanisms operating in the subconscious brain have been described in animals and humans (3) . However, eating is as much a means of achieving energy balance as it is a form of pleasure and reward. This makes the drive to eat one of the most powerful urges of animal and human behavior.
Reward, Addiction, and Food
The behavioral outcome of a reward is in making subjects "come back for more" by conditioning the approach and consumption activity to the hedonic feelings derived from the anticipation and attainment of the desired object (4) .
The parallel between drug dependence, which is the condition originally defined as addiction, and overeating, which leads to obesity, may not seem immediately apparent. Addiction is a chronically relapsing disorder characterized by compulsion to seek and take the drug; loss of control in limiting intake of the drug; and onset of a negative emotional state (e.g., anxiety, irritability) when access to the drug is prevented (i.e., dependence) (5) . In addicted drug users, craving is elicited by exposure to drug-related cues, which may trigger a relapse. A similar behavior characterizes the craving for food in overeaters (6) . It is known that eating disorders tend to cluster with drug and alcohol abuse in individuals and families (6) , and common neural circuits are thought to underlie food and drug rewards, including opioid (7) (8) (9) , serotoninergic (8) (9) , and dopaminergic pathways (8) (9) (10) . It has been proposed that the dopaminergic brain circuitry underlying addictions originally developed to subserve eating behavior (11) . However, whereas food is the most common and natural source of pleasure in everyday life and the neurophysiology of reward in humans has been extensively studied in the context of drug abuse (12) , little is known about how the human brain specifically processes food reward.
Role of Dopamine in Modulating Eating Behavior
[...]
However, the brain’s response to food reward is not likely to be confined to the striatum. Consistent with lesion studies in animals (9) , neuroimaging studies in humans have provided converging evidence that the central processing of food reward consistently overlaps with the sensory and visceral responses to ingestion of food in the insula, orbitofrontal cortex, and anteromedial temporal lobe (30) , areas that receive dopaminergic afferents through the mesolimbic and mesocortical pathways. Interestingly, in some of these areas, we observed a larger decrease of activity in obese compared with lean men (p < 0.001) (29) . Taken together, this evidence suggests that the cortical processing of food sensory cues participates in the motivational aspects of eating behavior. How this cortical processing may be affected by cognitive stimuli such as food advertisements in different communication media and how it may reinforce eating habits remain to be established.
Conclusions
Do we have enough new evidence from neurofunctional and other studies to begin to suspect that human obesity is predominantly an addictive disorder characterized by compulsive eating? We cannot say for sure, as yet. Some critical steps needed to further our understanding include establishing [as preliminary data seem to suggest (31) ] whether dopamine is released in response to food ingestion in humans (as it is in animals) and establishing the pathophysiological meaning of selective neurophysiological differences between obese and lean individuals. This may be accomplished by studying the brain and its dopaminergic pathways in individuals at high risk for the disease before they gain weight and become frankly obese. Nevertheless, we contend that more research on the role of the brain in the etiology of weight gain may help us understand if the current epidemic of obesity, which we are helplessly watching spread around the world, is a global case of food addiction.
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