The Addictive Dimensionality of Obesity
Open accessAbstract
Our brains are hardwired to respond and seek immediate rewards. Thus, it is not surprising that many people overeat, which in some can result in obesity, whereas others take drugs, which in some can result in addiction. Though food intake and body weight are under homeostatic regulation, when highly palatable food is available, the ability to resist the urge to eat hinges on self-control. There is no homeostatic regulator to check the intake of drugs (including alcohol); thus, regulation of drug consumption is mostly driven by self-control or unwanted effects (i.e., sedation for alcohol). Disruption in both the neurobiological processes that underlie sensitivity to reward and those that underlie inhibitory control can lead to compulsive food intake in some individuals and compulsive drug intake in others. There is increasing evidence that disruption of energy homeostasis can affect the reward circuitry and that overconsumption of rewarding food can lead to changes in the reward circuitry that result in compulsive food intake akin to the phenotype seen with addiction. Addiction research has produced new evidence that hints at significant commonalities between the neural substrates underlying the disease of addiction and at least some forms of obesity. This recognition has spurred a healthy debate to try and ascertain the extent to which these complex and dimensional disorders overlap and whether or not a deeper understanding of the crosstalk between the homeostatic and reward systems will usher in unique opportunities for prevention and treatment of both obesity and drug addiction.
AI snapshot
Written from the paper’s full text.
TL;DR
This review argues that obesity and addiction share neurobiological substrates—especially dopamine pathways—while also involving unique processes, so food reward is best viewed as a dimensional component of obesity rather than proof that obesity is food addiction. It synthesizes genetic, molecular, neurocircuitry, and behavioral overlaps to suggest that addiction prevention and treatment strategies may inform obesity interventions.
Key findings
- A genome-wide association study in 249,796 individuals of European descent identified 32 loci associated with BMI, but these explained only 1.5% of BMI variance. Candidate overlapping genes include DRD2 Taq I A1, CNR1, and the OPRM1 A118G polymorphism, linked to addiction, obesity risk, binge-eating, or alcoholism.
- Homeostatic and reward systems interact: VTA/NAc neurons express receptors for GLP-1, ghrelin, leptin, insulin, orexin, and melanocortins; orexigenic signals increase VTA DA cell activity to food stimuli, while anorexigenic signals inhibit DA firing and decrease DA release. Human data cited include an inverse relationship between BMI and illicit drug use, lower risk for substance use disorders in obese individuals, and increased risk for alcohol abuse/alcoholism relapse after bariatric surgery.
- Both addicted and obese subjects show blunted reward-circuit activation during consumption but sensitized responses to conditioned cues. Obese individuals viewing high-calorie food showed increased activation in NAc, dorsal striatum, OFC, ACC, amygdala, hippocampus, and insula; reduced striatal D2R availability is reported in addiction and obesity and is associated with decreased prefrontal activity.
- The insula is implicated in food, cocaine, and cigarette cravings; gastric distention activates the posterior insula, but lean—not obese—subjects showed amygdala activation and anterior insula deactivation. The extended amygdala, corticotropin-releasing factor signaling, and habenula are proposed to contribute to stress reactivity and the “dark side” transition in addiction and possibly food addiction.
Methods
- Narrative review and conceptual synthesis, not a systematic review or primary study. It integrates preclinical animal models and human genetic, imaging, and clinical evidence.
- The main analysis argues that homeostatic and reward systems interact, with dopamine as a common substrate across mesoaccumbens/mesolimbic, mesostriatal, and mesocortical pathways. It proposes a “bowtie”/nested layered architecture model in which the DA system subserves hypothalamic internal signals.
- Specific evidence cited includes a GWAS of 249,796 individuals, human PET/fMRI studies, rodent feeding and drug-reward experiments, and clinical observations such as bariatric surgery outcomes.
Limitations
- The authors state they do not claim obesity is the result of food addiction, but rather that food reward plays a critical role in overeating and obesity, referring to it as the dimensional component of obesity. They also note that the extent of overlap remains debated, that it is unclear whether obesogenic diets decrease striatal D2R, and that the extent of similar direct/indirect pathway regulatory processes in obesity remains unclear.
- Evident from the text: as a narrative review, it does not use a systematic search or quantitative synthesis, and many cited findings are correlational or from animal models, so causal direction and human generalizability are not fully established.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
0 of 120 cited sources checked · 0 supported · 0 flagged
- Interpretationreasoning
The explained BMI variance is unlikely to improve with larger samples due to complex biological-environmental interactions.
“However, these 32 loci explained only 1.5% of the BMI variance (1,2), a situation that is unlikely to improve with larger samples because of the complex interactions between biological and environmental factors.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [1] Naukkarinen, 2010, Use of genome-wide expression data to mine the “Gray Zone“ of GWA studies leads to novel candidate obesity genes, PLoS Genet source
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- cites [2] Speliotes, 2010, Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index, Nat Genet source
Not checked in the free run.
- Interpretationreasoning
The dopamine system, via mesoaccumbens/mesolimbic, mesostriatal, and mesocortical pathways, is a common substrate in the neurobiology of both addiction and obesity.
“Thus, the dopamine (DA) system, through the mesoaccumbens/mesolimbic (reward and emotions), mesostriatal (habits, routines, and movement), and mesocortical (executive function) pathways, is a common substrate in the neurobiology of both disorders (Figure 1).”
Quote in the paperSubstantial claim - Premisecitation
Several hormones and neuropeptides involved in energy homeostasis influence the DA reward pathway.
“Specifically, several hormones and neuropeptides involved in energy homeostasis influence the DA reward pathway (9).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9] Volkow, 2013, Obesity and addiction: Neurobiological overlaps, Obes Rev source
Not checked in the free run.
- Interpretationreasoning
Addiction research has produced evidence of significant commonalities between neural substrates of addiction and at least some forms of obesity.
“Addiction research has produced new evidence that hints at significant commonalities between the neural substrates underlying the disease of addiction and at least some forms of obesity.”
Quote in the paperSubstantial claim - Premisecitation
A GWAS of 249,796 individuals of European descent identified 32 loci associated with BMI.
“Indeed, the most recent whole genome-wide association study conducted in 249,796 individuals of European descent identified 32 loci associated with body mass index (BMI).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [1] Naukkarinen, 2010, Use of genome-wide expression data to mine the “Gray Zone“ of GWA studies leads to novel candidate obesity genes, PLoS Genet source
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- cites [2] Speliotes, 2010, Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index, Nat Genet source
Not checked in the free run.
- Premisecitation
Those 32 loci explained only 1.5% of BMI variance.
“However, these 32 loci explained only 1.5% of the BMI variance (1,2), a situation that is unlikely to improve with larger samples because of the complex interactions between biological and environmental factors.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [1] Naukkarinen, 2010, Use of genome-wide expression data to mine the “Gray Zone“ of GWA studies leads to novel candidate obesity genes, PLoS Genet source
Not checked in the free run.
- cites [2] Speliotes, 2010, Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index, Nat Genet source
Not checked in the free run.
- Interpretationreasoning
Both addiction and obesity reflect imbalances in brain responses to rewarding environmental stimuli.
“Both addiction and obesity reflect imbalances in the responses of the brain to rewarding stimuli in the environment.”
Quote in the paperSubstantial claim - Interpretationreasoning
Disruption in reward sensitivity and inhibitory control processes can lead to compulsive food intake in some individuals and compulsive drug intake in others.
“Disruption in both the neurobiological processes that underlie sensitivity to reward and those that underlie inhibitory control can lead to compulsive food intake in some individuals and compulsive drug intake in others.”
Quote in the paperSubstantial claim - Interpretationnone given
Obesity's reward imbalance can be triggered by endocrinological abnormalities that alter energetic threshold and food reward sensitivity.
“For obesity, this imbalance can be triggered by endocrinological abnormalities that change the energetic threshold and modify the sensitivity to food rewards.”
Quote in the paperNot a substantial claim - Premisenone given
Eating decisions are influenced by nonhomeostatic factors such as food palatability and environmental cues that trigger conditioned responses.
“The decision to eat (or not) is not only influenced by the internal state of the caloric equation but also by nonhomeostatic factors, such as food palatability and environmental cues that trigger conditioned responses.”
Quote in the paperSubstantial claim - Premisecitation
With repeated exposure, DA neurons stop firing when receiving food and instead fire to the stimulus predicting food delivery.
“With repeated exposure, the DA neurons stop firing when receiving the food and fire instead when exposed to the stimulus that predicts food delivery (33).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [33] Schultz, 1998, Predictive reward signal of dopamine neurons, J Neurophysiol source
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- Premisecitation
In obese individuals with binge-eating disorder, higher DA release when exposed to food cues is associated with disorder severity.
“Similarly, in obese individuals with binge-eating disorder, higher DA release—when exposed to food cues—was associated with the severity of the disorder (51).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [51] Wang, 2011, Enhanced striatal dopamine release during food stimulation in binge eating disorder, Obesity (Silver Spring) source
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- Interpretationreasoning
These hormones/peptides can influence rewarding responses to drugs of abuse.
“Therefore, it is not surprising that these hormone/peptides can influence the rewarding responses to drugs of abuse.”
Quote in the paperSubstantial claim - Premisecitation
Projections from amygdala, hippocampus, and OFC to DA neurons and NAc are involved in conditioned responses to food and drugs.
“More specifically, projections from the amygdala, hippocampus, and OFC to DA neurons and to NAc are involved in conditioned responses to food (52) and drugs (53).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [52] Petrovich, 2010, Forebrain circuits and control of feeding by learned cues, Neurobiol Learn Mem source
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- cites [53] Lasseter, 2011, Interaction of the basolateral amygdala and orbitofrontal cortex is critical for drug context-induced reinstatement of cocaine-seeking behavior in rats, Neuropsychopharmacology source
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- Premisereasoning
DA neurons in VTA and substantia nigra modulate reward and the motivation and sustainability of effort needed for survival behaviors.
“Dopamine neurons (both in VTA and substantia nigra) modulate not only reward but also the motivation and sustainability of effort necessary to accomplish behaviors needed for survival.”
Quote in the paperSubstantial claim - Premisecitation
Rodent experiments show DA signaling through D1 and D2 receptors in dorsal striatum is necessary for feeding and eating-related behaviors.
“Experiments in rodents have shown, for example, that DA signals through both D1 receptors and D2 receptors (D2R) in the dorsal striatum are necessary for feeding and other eating-related behaviors (28).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [28] Palmiter, 2008, Dopamine signaling in the dorsal striatum is essential for motivated behaviors: Lessons from dopamine-deficient mice, Ann N Y Acad Sci source
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- Interpretationreasoning
Palatable foods, like drugs of abuse, are powerful environmental triggers that in vulnerable individuals can facilitate or exacerbate uncontrolled behaviors.
“Thus, palatable foods, like drugs of abuse, represent a powerful environmental trigger, which, in vulnerable individuals, has the potential to facilitate or exacerbate the establishment of uncontrolled behaviors.”
Quote in the paperSubstantial claim - Premisecitation
Many neurotransmitters implicated in drug-seeking behaviors are also implicated in food intake.
“Predictably then, many neurotransmitters implicated in drug-seeking behaviors are also implicated in food intake (9).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9] Volkow, 2013, Obesity and addiction: Neurobiological overlaps, Obes Rev source
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- Premisecitation
Animal models show that after extinction, drug or food consumption behavior can be triggered by cue, reward, or stressor.
“Animal models of both food and drug reward have shown that after extinction, the behavior for drug or food consumption can be triggered either by exposure to the cue, the reward, or a stressor (34).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [34] Nair, 2009, The neuropharmacology of relapse to food seeking: Methodology, main findings, and comparison with relapse to drug seeking, Prog Neurobiol source
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- Premisecitation
Preclinical studies showing decreased VTA DA activity causes dramatic increase in high-fat food consumption partially support the compensation hypothesis.
“Preclinical studies showing that decreased DA activity in VTA results in a dramatic increase in the consumption of high-fat foods (47) partially support this hypothesis.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [47] Stoeckel, 2008, Widespread reward-system activation in obese women in response to pictures of high-calorie foods, Neuroimage source
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- Premisecitation
Compared with normal-weight individuals, obese individuals viewing high-calorie food pictures show increased activation in reward and motivation circuits (NAc, dorsal striatum, OFC, ACC, amygdala, hippocampus, insula).
“Compared with normal-weight individuals, obese individuals observing pictures of high-calorie food (stimuli to which they are conditioned) showed increased activation in regions of the reward and motivation circuits (NAc, dorsal striatum, orbitofrontal cortex [OFC], anterior cingulate cortex [ACC], amygdala, hippocampus, and insula) (50).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [50] Killgore, 2005, Body mass predicts orbitofrontal activity during visual presentations of high-calorie foods, Neuroreport source
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- Premisecitation
Both addicted and obese subjects show sensitized responses to conditioned cues predictive of drug or food reward.
“In contrast to the blunted reward responses during reward consumption, both addicted and obese subjects show sensitized responses to conditioned cues predictive of drug or food reward.”
Quote in the paperSubstantial claim - Premisenone given
When a cue does not lead to expected food reward, DA neuron activity is inhibited, decreasing the incentive value of the cue (extinction).
“Interestingly, when the cue does not lead to the expected food reward, DA neuron activity is inhibited, decreasing the incentive value for the cue (extinction).”
Quote in the paperNot a substantial claim - Interpretationreasoning
The neurocircuitry model of addiction also applies to certain types of obesity.
“It can be argued that this neurocircuitry model of addiction also applies to certain types of obesity.”
Quote in the paperNot a substantial claim - Premisecitation
Drugs of abuse tap into the same neuronal mechanisms that modulate motivation and drive to seek and consume food.
“The phenomenological and neurobiological overlaps between obesity and addiction can be predicted on the basis that drugs of abuse tap into the same neuronal mechanisms that modulate the motivation and drive to seek and consume food (27).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [27] Volkow, 2007, Issues for DSM-V: Should obesity be included as a brain disorder?, Am J Psychiatry source
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- Premisecitation
The urge to seek and consume drugs in addiction involves disruption of reward circuitry and other circuits including interoception, inhibitory control, mood/stress regulation, and memory.
“The overwhelming urge to seek and consume the drug in addiction involves disruption not only of the reward circuitry but also of other circuits, including interoception, inhibitory control, mood and stress regulation, and memory (39).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [39] Volkow, 2010, Addiction: Decreased reward sensitivity and increased expectation sensitivity conspire to overwhelm the brain's control circuit, Bioessays source
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- Interpretationreasoning
These results suggest that food and drugs may compete for overlapping reward mechanisms.
“Taken together, these results strongly suggest the possibility that food and drugs may be competing for overlapping reward mechanisms.”
Quote in the paperSubstantial claim - Premisecitation
For drug reward, an imbalance between enhanced D1 and decreased D2 receptor signaling facilitates compulsive drug intake.
“For drug reward, studies have also shown that an imbalance between D1 receptor signaling (enhanced) and D2 receptor signaling (decreased) facilitates compulsive drug intake (36);”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [36] Luo, 2011, Acute cocaine induces fast activation of D1 receptor and progressive deactivation of D2 receptor striatal neurons: In vivo optical microprobe [Ca2+]i imaging, J Neurosci source
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- Premisecitation
Glutamatergic afferents to DA neurons from reward, conditioning, and salience regions modulate their activity in response to conditioned cues.
“The extensive glutamatergic afferents to DA neurons from regions involved in the processing of reward (NAc), conditioning (amygdala, hippocampus, prefrontal cortex), and salience attribution (orbitofrontal cortex) modulate their activity in response to conditioned cues (31).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [31] Geisler, 2008, Functional implications of glutamatergic projections to the ventral tegmental area, Rev Neurosci source
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- Premisecitation
Bariatric surgery for obesity is associated with increased risk for relapse to alcohol abuse and alcoholism.
“and bariatric surgery for obesity is associated with an increased risk for relapse to alcohol abuse and alcoholism (26).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [26] Suzuki, 2012, Alcohol use disorders after bariatric surgery, Obes Surg source
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- Premisecitation
Repeated drug exposures are associated with long-lasting reductions in striatal D2R levels and signaling in preclinical studies.
“Similarly, preclinical studies have shown that repeated drug exposures are associated with long-lasting reductions in striatal D2R levels and signaling (72,73).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [72] Nader, 2006, PET imaging of dopamine D2 receptors during chronic cocaine self-administration in monkeys, Nat Neurosci source
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- cites [73] Volkow, 2001, Low level of brain dopamine D2 receptors in methamphetamine abusers: Association with metabolism in the orbitofrontal cortex, Am J Psychiatry source
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- Premisenone given
Drug cues are more powerful triggers of reinforcer-seeking behavior after abstinence than food cues.
“However, compared with food cues, drug cues are more powerful triggers of reinforcer-seeking behavior following a period of abstinence.”
Quote in the paperSubstantial claim - Premisecitation
The capacity to inhibit prepotent responses and exert self-control contributes to suppressing inappropriate behaviors like drug taking or eating past satiety, modulating vulnerability to addiction or obesity.
“The capacity to inhibit prepotent responses and exert self-control contributes to an individual’s ability to suppress inappropriate behaviors, such as taking drugs or eating past the point of satiety, thus modulating the vulnerability to addiction or obesity, respectively (70,71).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [70] Volkow, 2000, Addiction, a disease of compulsion and drive: Involvement of the orbitofrontal cortex, Cereb Cortex source
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- cites [71] Volkow, 2008, Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: Possible contributing factors, Neuroimage source
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- Premisecitation
Once extinguished, drug-reinforced behaviors are more susceptible to stress-induced reinstatement than food-reinforced behaviors.
“Thus, once extinguished, drug-reinforced behaviors are far more susceptible to stress-induced reinstatement than food-reinforced behaviors (56).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [56] Kearns, 2011, A review of preclinical research demonstrating that drug and non-drug reinforcers differentially affect behavior, Curr Drug Abuse Rev source
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- Interpretationcitation
Improper D2R-mediated DA regulation of frontal regions in addicted and obese subjects could underlie enhanced incentive motivational value of drugs/food and difficulty resisting them.
“Thus, improper regulation by D2R-mediated DA signaling of these frontal regions in addicted and obese subjects could underlie the enhanced incentive motivational value of drugs or food and the difficulty in resisting them (70,71).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [70] Volkow, 2000, Addiction, a disease of compulsion and drive: Involvement of the orbitofrontal cortex, Cereb Cortex source
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- cites [71] Volkow, 2008, Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: Possible contributing factors, Neuroimage source
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- Premisecitation
The reduction in striatal D2R in addiction and obesity is associated with decreased activity in prefrontal regions involved in salience attribution (OFC), error detection/inhibition (ACC), and decision making (dlPFC).
“The reduction in striatal D2R in addiction and in obesity is associated with decreased activity in prefrontal regions involved in salience attribution (OFC), error detection and inhibition (ACC), and decision making (dorsolateral prefrontal cortex) (73,79,80).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [73] Volkow, 2001, Low level of brain dopamine D2 receptors in methamphetamine abusers: Association with metabolism in the orbitofrontal cortex, Am J Psychiatry source
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- cites [79] Volkow, 1993, Decreased dopamine D2 receptor availability is associated with reduced frontal metabolism in cocaine abusers, Synapse source
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- cites [80] Volkow, 2007, Profound decreases in dopamine release in striatum in detoxified alcoholics: Possible orbitofrontal involvement, J Neurosci source
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- Premisecitation
Cue-conditioned cravings and incentive motivation for food also occur in healthy individuals who do not overeat.
“The emergence of cue-conditioned cravings and incentive motivation for the reward, which for food also occur in healthy individuals who do not overeat (69), would not be as devastating were they not coupled with growing deficits in the brain’s ability to inhibit maladaptive behaviors.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [69] Volkow, 2002, “Nonhedonic“ food motivation in humans involves dopamine in the dorsal striatum and methylphenidate amplifies this effect, Synapse source
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- Premisecitation
Normal-weight subjects exposed to food cues show increased OFC activity associated with food craving.
“Normal-weight subjects exposed to food cues showed increased activity in OFC, which was associated with food craving (63).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [63] Wang, 2004, Exposure to appetitive food stimuli markedly activates the human brain, Neuroimage source
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- Premisecitation
Similar inhibition of OFC and NAc activity was observed in cocaine abusers inhibiting drug craving during cocaine cues.
“A similar inhibition of OFC activity (and NAc) was observed in cocaine abusers when they were asked to inhibit their drug craving during exposure to cocaine cues (55).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Volkow, 2009, Cognitive control of drug craving inhibits brain reward regions in cocaine abusers, Neuroimage source
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- Premisenone given
Preclinical and clinical studies suggest impairments in striatal DA signaling may undermine self-control.
“Preclinical and clinical studies have suggested that impairments in striatal DA signaling may undermine self-control as described below.”
Quote in the paperNot a substantial claim - Premisecitation
Successful dieters activate prefrontal regions involved in inhibitory control (dlPFC and OFC) while eating.
“Interestingly, successful dieters activate prefrontal regions involved in inhibitory control (dorsolateral prefrontal cortex and OFC) while eating (88).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [88] DelParigi, 2007, Successful dieters have increased neural activity in cortical areas involved in the control of behavior, Int J Obes (Lond) source
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- Interpretationreasoning
Studies show a correlation between executive function and addiction and obesity risk/phenotypes.
“These and other studies evince a correlation between executive function and addiction and obesity risk/phenotypes, and further research will help clarify details as well as differences between these phenotypes.”
Quote in the paperSubstantial claim - Premisecitation
In humans, tasting palatable foods activated the insula and midbrain areas.
“Indeed, in humans, tasting palatable foods activated the insula and midbrain areas (102,103).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [102] DelParigi, 2005, Sensory experience of food and obesity: A positron emission tomography study of the brain regions affected by tasting a liquid meal after a prolonged fast, Neuroimage source
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- cites [103] Frank, 2008, Sucrose activates human taste pathways differently from artificial sweetener, Neuroimage source
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- Premisecitation
In drug addiction and in some cases of obesity or eating disorders, stress and negative moods such as depression and anxiety can trigger compulsive drug or food intake in humans.
“They pointed out that both in drug addiction and in certain instances of obesity or eating disorders, stress and negative moods (depression, anxiety) can trigger compulsive drug (in addiction) or food intake in humans (obesity and eating disorders).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [106] Parylak, 2011, The dark side of food addiction, Physiol Behav source
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- Premisecitation
A cross-sectional study of children found executive function proficiency negatively correlated with substance use, high-calorie snack consumption, and sedentary behaviors.
“Interestingly, a cross-sectional investigation of children’s ability to self-regulate, solve problems, and engage in goal-directed health behaviors revealed executive function proficiency to be negatively correlated not only with substance use but also with the consumption of high-calorie snack foods and with sedentary behaviors (90).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [90] Riggs, 2012, Relationships between executive cognitive function and lifetime substance use and obesity-related behaviors in fourth grade youth, Child Neuropsychol source
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- Premisecitation
DA is involved in responses to tasting palatable foods mediated through the insula.
“Even though the modulation of insular activity by DA has been poorly investigated, it is recognized that DA is involved in responses to the tasting of palatable foods that are mediated through the insula (101).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [101] Hajnal, 2005, Taste pathways that mediate accumbens dopamine release by sapid sucrose, Physiol Behav source
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- Premisecitation
Insula reactivity has been suggested as a biomarker to predict relapse.
“Accordingly, the reactivity of the insula has been suggested as a biomarker to help predict relapse (96).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [96] Janes, 2010, Brain reactivity to smoking cues prior to smoking cessation predicts ability to maintain tobacco abstinence, Biol Psychiatry source
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- Premisecitation
A recent study of siblings discordant for stimulant addiction found addicted siblings had significantly smaller OFC than nonaddicted siblings or controls.
“Interestingly, a recent study of siblings discordant for their addiction to stimulant drugs found that the OFC of the addicted siblings was significantly smaller than that of nonaddicted siblings or control subjects (82).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [82] Ersche, 2012, Abnormal brain structure implicated in stimulant drug addiction, Science source
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- Premisecitation
The middle insula plays a critical role in cravings for food, cocaine, and cigarettes.
“The middle insula plays a critical role in cravings for food, cocaine, and cigarettes (91–93).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [91] Bonson, 2002, Neural systems and cue-induced cocaine craving, Neuropsychopharmacology source
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- cites [92] Pelchat, 2004, Images of desire: Food-craving activation during fMRI, Neuroimage source
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- cites [93] Wang, 2007, Neural substrates of abstinence-induced cigarette cravings in chronic smokers, J Neurosci source
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- Premisecitation
The rostral insula provides information to the OFC that influences its multimodal representation of pleasantness or reward value of incoming food.
“In addition, the rostral insula (connected to primary taste cortex) provides information to the OFC that influences its multimodal representation of the pleasantness or reward value of incoming food (97).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [97] Rolls, 2008, Functions of the orbitofrontal and pregenual cingulate cortex in taste, olfaction, appetite and emotion, Acta Physiol Hung source
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- Premisecitation
Many imaging studies show differential activation of the insula during craving.
“Consistent with this hypothesis, many imaging studies show differential activation of the insula during craving (95).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [95] Naqvi, 2009, The hidden island of addiction: The insula, Trends Neurosci source
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- Premisecitation
Smokers who suffered a stroke damaging the insula were able to quit easily without cravings or relapse.
“Its importance in addiction was highlighted when a study found that smokers who suffered a stroke that damaged the insula were able to quit easily and without experiencing either cravings or relapse (94).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [94] Naqvi, 2007, Damage to the insula disrupts addiction to cigarette smoking, Science source
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- Interpretationreasoning
The lack of amygdalar response in obese subjects could reflect blunted interoceptive awareness of satiety-related bodily states.
“The lack of amygdalar response in obese subjects could reflect a blunted interoceptive awareness of bodily states linked with satiety (full stomach).”
Quote in the paperSubstantial claim - Premisecitation
In healthy controls, BMI was negatively correlated with metabolic activity in prefrontal regions whose activity predicted executive function test scores.
“Similarly, in healthy control subjects, BMI was negatively correlated with metabolic activity in prefrontal regions for which the activity predicted the scores on tests of executive function (87).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [87] Volkow, 2009, Inverse association between BMI and prefrontal metabolic activity in healthy adults, Obesity (Silver Spring) source
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- Interpretationcitation
Brain imaging data support that structural and functional changes in executive/inhibitory brain regions are associated with high BMI in otherwise healthy individuals.
“Brain imaging data also support the notion that structural and functional changes in brain regions implicated in executive (including inhibitory) function are associated with high BMI in otherwise healthy individuals.”
Quote in the paperSubstantial claim - Premisecitation
Obese subjects exhibit greater insular activation than normal controls when tasting a liquid meal with sugar and fat.
“Obese subjects exhibit greater insular activation than normal control subjects when tasting a liquid meal with sugar and fat (102).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [102] DelParigi, 2005, Sensory experience of food and obesity: A positron emission tomography study of the brain regions affected by tasting a liquid meal after a prolonged fast, Neuroimage source
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- Interpretationnone given
DA signaling appears necessary for sensing the calorie content of food.
“In addition, DA signaling appears to also be necessary for sensing the calorie content of food.”
Quote in the paperNot a substantial claim - Interpretationcitation
Individual differences in executive function can constitute a prodromal risk for later obesity in some individuals.
“Clearly, individual differences in executive function can constitute a prodromal risk for later obesity in some individuals (89).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [89] Riggs, 2012, Executive function and latent classes of childhood obesity risk, J Behav Med source
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- Premisecitation
Gastric distention activates the posterior insula, likely reflecting awareness of body states such as fullness.
“Indeed, gastric distention results in activation of the posterior insula, a likely reflection of its role in the awareness of body states (in this case of fullness) (99).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [99] Wang, 2008, Gastric distention activates satiety circuitry in the human brain, Neuroimage source
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- Premisecitation
In lean but not obese subjects, gastric distention activated the amygdala and deactivated the anterior insula.
“Moreover, in lean but not in obese subjects, gastric distention resulted in activation of the amygdala and deactivation of the anterior insula (100).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [100] Tomasi, 2009, Association of body mass and brain activation during gastric distention: Implications for obesity, PLoS One source
Not checked in the free run.
- Interpretationreasoning
Eating behaviors exemplify the bowtie architecture, with the hypothalamus as a central knot of the metabolic bowtie.
“Eating behaviors present a great example of this architecture where the hypothalamus is a central knot of the metabolic bowtie (Figure 2A)”
Quote in the paperSubstantial claim - Premisecitation
The Parylak model emphasizes brain circuits that modulate stress reactivity and antireward, which are enhanced after repeated drug exposures and after intermittent access to palatable foods.
“Their model highlights the importance of brain circuits that modulate stress reactivity and antireward, which are enhanced after repeated drug exposures but also after intermittent access to palatable foods.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [106] Parylak, 2011, The dark side of food addiction, Physiol Behav source
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- Interpretationcitation
The metabolic and dopamine systems are examples of nested layered architectures in which the dopamine bowtie subserves internal signals mediated by hypothalamic signaling.
“These two systems can be viewed as examples of nested layered architectures (111), in which the DA bowtie subserves the internal signals mediated by hypothalamic signaling (Figure 2C).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [111] Csete, 2004, Bow ties, metabolism and disease, Trends Biotechnol source
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- Interpretationreasoning
The lateral habenula likely mediates responses to aversive stimuli or states such as dieting or drug withdrawal.
“These findings are consistent with a role for the lateral habenula in mediating responses to aversive stimuli or states such as those that occur during dieting or drug withdrawal.”
Quote in the paperSubstantial claim - Interpretationreasoning
Midbrain dopamine nuclei (VTA and substantia nigra) and their projection regions form a central knot for a system that reacts to salient external stimuli, including drugs and food, and to internal signals such as hunger and thirst.
“and midbrain DA nuclei (VTA and substantia nigra) and their projection regions (NAc; amygdala; hippocampus; dorsal striatum; and prefrontal, motor, and temporal cortices) represent a central knot for a system that reacts to salient external stimuli (including drugs and food), as well as relevant internal signals (i.e., hunger, thirst) (Figure 2B).”
Quote in the paperSubstantial claim - Premisecitation
The habenula inhibits VTA dopamine neuron firing when an expected reward does not occur.
“In parallel, the recognition that the habenula mediates inhibition of VTA DA neuron firing when an expected reward does not materialize (107) also implicates this region in contributing to such antireward circuitry.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [107] Kimura, 2007, What does the habenula tell dopamine neurons?, Nat Neurosci source
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- Premisecitation
The human brain is organized as a layered architecture of interactive networks, sometimes called a bowtie, in which many inputs converge onto a small number of processes and then fan out into diverse outputs.
“The human brain is a complex biological system that is organized in the layered architecture of interactive networks, sometimes called bowtie (111), whereby a narrowing funnel of many potential inputs converges onto a relatively small number of processes before fanning out again into a diversity of outputs.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [111] Csete, 2004, Bow ties, metabolism and disease, Trends Biotechnol source
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- Premisecitation
In animal models of cocaine or heroin addiction, activation of the lateral habenula is associated with relapse.
“Indeed, activation of the lateral habenula, in animal models of cocaine or heroin addiction, has been associated with relapse (108,109).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [108] Zhang, 2005, Increased c-Fos expression in the medial part of the lateral habenula during cue-evoked heroin-seeking in rats, Neurosci Lett source
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- cites [109] Brown, 2011, Identification of brain nuclei implicated in cocaine-primed reinstatement of conditioned place preference: A behaviour dissociable from sensitization, PLoS One source
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- May combine two claims. 55
- Classified as probably not a substantial claim. 10
May combine two claims.
FindingcitationSubjects with high genetic risk for alcoholism who were not alcoholic had higher than normal striatal D2R associated with normal prefrontal metabolism, which might have protected them.
“Indeed, we showed that subjects who, despite having a high genetic risk for alcoholism (positive family history of alcoholism) were not alcoholics, had higher than normal striatal D2R, which was associated with normal prefrontal metabolism (81) that might have protected them from alcoholism.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [81] Volkow, 2006, High levels of dopamine D2 receptors in unaffected members of alcoholic families: Possible protective factors, Arch Gen Psychiatry source
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Interpretationnone givenObesity can result from easy access to highly palatable food, and excessive consumption of such food can affect homeostatic signaling and disrupt food reward sensitivity.
“However, obesity can also result from easy access to highly palatable food, excessive consumption of which can affect homeostatic signaling and disrupt the sensitivity to food reward.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningFood reward plays a critical role in overeating and obesity, which the authors call the dimensional component of obesity.
“We present evidence of shared neurobiological substrates and do not claim that obesity is the result of food addiction but rather that food reward plays a critical role in overeating and obesity, referring to it as the dimensional component of obesity.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationVTA and/or NAc neurons express receptors for GLP-1, ghrelin, leptin, insulin, orexin, and melanocortin.
“Moreover, neurons in VTA and/or nucleus accumbens (NAc) express glucagon-like peptide-1 (11,12), ghrelin (13,14), leptin (15,16), insulin (17), orexin (18), and melanocortin receptors (19).”
Quote in the paperSubstantial claim0 of 6 sources checked- cites [11] Alhadeff, 2012, GLP-1 neurons in the nucleus of the solitary tract project directly to the ventral tegmental area and nucleus accumbens to control for food intake, Endocrinology source
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- cites [12] Rinaman, 2010, Ascending projections from the caudal visceral nucleus of the solitary tract to brain regions involved in food intake and energy expenditure, Brain Res source
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- cites [13] Abizaid, 2006, Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite, J Clin Invest source
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- cites [14] Jerlhag, 2007, Ghrelin administration into tegmental areas stimulates locomotor activity and increases extracellular concentration of dopamine in the nucleus accumbens, Addict Biol source
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- cites [15] Figlewicz, 2003, Expression of receptors for insulin and leptin in the ventral tegmental area/substantia nigra (VTA/SN) of the rat, Brain Res source
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- cites [16] Leshan, 2010, Ventral tegmental area leptin receptor neurons specifically project to and regulate cocaine- and amphetamine-regulated transcript neurons of the extended central amygdala, J Neurosci source
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Premisenone givenDrug intake lacks a homeostatic regulator, so drug consumption is mostly regulated by self-control or unwanted effects.
“There is no homeostatic regulator to check the intake of drugs (including alcohol); thus, regulation of drug consumption is mostly driven by self-control or unwanted effects (i.e., sedation for alcohol).”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationObesity is associated with genes involved in DA neurotransmission, such as DRD2 Taq I A1 allele, which is also associated with addiction.
“This could explain the association of obesity with genes involved with DA neurotransmission, such as the DRD2 Taq I A1 allele, which has been associated with addiction (4).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [4] Blum, 1996, Increased prevalence of the Taq I A1 allele of the dopamine receptor gene (DRD2) in obesity with comorbid substance use disorder: A preliminary report, Pharmacogenetics source
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Probably not a substantial claim: may not pass S4 (based).
Premisenone givenRepeated drug consumption can directly disrupt the reward circuit, its main pharmacological target.
“Repeated consumption of a drug, on the other hand, can directly disrupt the reward circuit, its main pharmacologic target.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationCNR1 gene variations have been associated with BMI and obesity risk by most studies, and with addiction.
“Similarly, there are genes at the intersection between reward and homeostatic pathways, like the cannabinoid receptor 1 (CNR1) gene, variations in which have been associated with BMI and obesity risk by most studies (5), as well as with addiction (6).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [5] Schleinitz, 2010, Role of genetic variation in the cannabinoid type 1 receptor gene (CNR1) in the pathophysiology of human obesity, Pharmacogenomics source
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- cites [6] Benyamina, 2010, CNR1 gene polymorphisms in addictive disorders: A systematic review and a meta-analysis, Addict Biol source
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PremisereasoningFood intake and body weight are homeostatically regulated, but when highly palatable food is available, resisting eating depends on self-control.
“Though food intake and body weight are under homeostatic regulation, when highly palatable food is available, the ability to resist the urge to eat hinges on self-control.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationOrexigenic signals increase VTA DA cell activity in response to food stimuli, while anorexigenic signals inhibit DA firing and decrease DA release.
“Overall, homeostatic orexigenic signals increase the activity of ventral tegmental area (VTA) DA cells when exposed to food stimuli, whereas anorexigenic ones inhibit DA firing and decrease DA release (10).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [10] Opland, 2011, Modulation of the mesolimbic dopamine system by leptin, Brain Res source
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PremisecitationEndogenous opioids are involved in hedonic responses to food and drugs, and the OPRM1 A118G polymorphism is associated with vulnerability to binge-eating disorders and alcoholism.
“And, let us also remember in this context that endogenous opioids are involved in hedonic responses to food and to drugs and that the functional A118G polymorphism in the μ-opioid receptor gene (OPRM1) has been associated with vulnerability for binge-eating disorders (7) and alcoholism (8).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [7] Davis, 2009, Dopamine for “wanting“ and opioids for “liking“: A comparison of obese adults with and without binge eating, Obesity (Silver Spring) source
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- cites [8] Ray, 2011, The role of the Asn40Asp polymorphism of the mu opioid receptor gene (OPRM1) on alcoholism etiology and treatment: A critical review, Alcohol Clin Exp Res source
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Interpretationnone givenDisruption of energy homeostasis can affect reward circuitry, and overconsumption of rewarding food can change reward circuitry to produce compulsive food intake similar to addiction.
“There is increasing evidence that disruption of energy homeostasis can affect the reward circuitry and that overconsumption of rewarding food can lead to changes in the reward circuitry that result in compulsive food intake akin to the phenotype seen with addiction.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationreasoningThe authors propose that addiction and obesity share neurobiological processes that when disrupted can cause compulsive consumption, while also having unique processes.
“We propose that these two diseases share neurobiological processes that, when disrupted, can result in compulsive consumption, while also involving unique neurobiological processes.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.
Premisenone givenHigh-calorie food is widely available not only as nutrition but also as a strong reward that promotes eating.
“This is particularly true whenever high-calorie content food is widely available, not just as a source of nutrition, but also as a strong reward that, by itself, promotes eating.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationThe magnitude of DA increases in addicted subjects predicts intensity of cue-induced cravings, and in animals predicts effort to get drug.
“The magnitude of these DA increases in addicted subjects predicts the intensity of cue-induced cravings (48), and in animals, they predict the effort that an animal is willing to exert to get the drug (49).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [48] Volkow, 2006, Cocaine cues and dopamine in dorsal striatum: Mechanism of craving in cocaine addiction, J Neurosci source
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- cites [49] Vanderschuren, 2005, Involvement of the dorsal striatum in cue-controlled cocaine seeking, J Neurosci source
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PremisecitationHuman studies found an inverse relationship between BMI and illicit drug use and lower risk for substance use disorders in obese individuals, including lower rates of nicotine and marijuana abuse.
“Similarly, human studies found an inverse relationship between BMI and illicit drug use (21) and a lower risk for substance use disorders in obese individuals (22), including lower rates of nicotine (23) and marijuana (24) abuse.”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [21] Bluml, 2012, Relationship between substance use and body mass index in young males, Am J Addict source
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- cites [22] Simon, 2006, Association between obesity and psychiatric disorders in the US adult population, Arch Gen Psychiatry source
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- cites [23] Blendy, 2005, Reduced nicotine reward in obesity: Cross-comparison in human and mouse, Psychopharmacology (Berl) source
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InterpretationreasoningDrugs activate brain reward pathways more potently than food, which helps explain their greater ability to induce loss of control and compulsive consumption.
“Since drugs activate brain reward pathways more potently than food, this helps explain (together with homeostatic satiety mechanisms) the greater ability of drugs to induce loss of control and compulsive consummatory behavior.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationOn first exposure to food reward, VTA DA neuron firing increases and DA release in NAc increases.
“For example, upon first exposure to a food reward, the firing of DA neurons in the VTA increases with a resulting increase in DA release in the NAc (32).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [32] Norgren, 2006, Gustatory reward and the nucleus accumbens, Physiol Behav source
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PremisecitationA D1-like antagonist blocked and a D2-like antagonist increased reinstatement of food-seeking behavior.
“This possibility is consistent with a recent report in which a D1-like antagonist blocked and a D2-like antagonist increased the reinstatement of food-seeking behavior (37).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [37] Ball, 2011, Opposing roles for dopamine D1- and D2-like receptors in discrete cue-induced reinstatement of food seeking, Behav Brain Res source
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PremisecitationBoth addicted and obese subjects show less activation of reward circuits when given the drug or palatable food, respectively.
“Surprisingly, both addicted and obese subjects exhibit less activation of reward circuits when given the drug or the palatable food, respectively (45).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [45] Stice, 2008, Relation of reward from food intake and anticipated food intake to obesity: A functional magnetic resonance imaging study, J Abnorm Psychol source
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InterpretationreasoningIncreases in DA induced by a conditioned stimulus predict the behavioral price an animal will pay to receive it, ensuring motivational drive occurs before eating.
“Moreover, since the increases in DA induced by the conditioned stimulus predict the behavioral price the animal is willing to pay to receive it, this will ensure that the motivational drive (fueled by DA signaling) occurs before the animal is eating the food itself.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationDA-deficient mice die of starvation likely due to decreased motivation to consume food, and replenishing dorsal striatum DA restores feeding and rescues them.
“Indeed, DA-deficient mice die of starvation, likely as a result of a decreased motivation to consume the food, and replenishing the dorsal striatum with DA restores feeding and rescues them (28).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [28] Palmiter, 2008, Dopamine signaling in the dorsal striatum is essential for motivated behaviors: Lessons from dopamine-deficient mice, Ann N Y Acad Sci source
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PremisecitationAnorexigenic peptides decrease brain reward system sensitivity to food reward, while orexigenic peptides increase it.
“Consistent with preclinical studies, imaging studies have also shown that anorexigenic peptides (e.g., insulin, leptin, peptide YY) decrease the sensitivity of the brain reward system to food reward, whereas orexigenic ones (e.g., ghrelin,) increase it [see review (44)].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [44] Volkow, 2011, Reward, dopamine and the control of food intake: Implications for obesity, Trends Cogn Sci source
Not checked in the free run.
Probably not a substantial claim: may not pass S4 (based). May combine two claims.
Premisenone givenDrugs of abuse activate the DA reward circuit, which if chronic in vulnerable individuals can result in addiction.
“Drugs of abuse work by activating the DA reward circuit, which, if chronic, in vulnerable individuals, can result in addiction.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisereasoningHigh-calorie foods can promote overeating uncoupled from energetic needs and trigger learned stimulus-reward associations.
“Indeed, high-calorie foods can promote overeating (i.e., eating that is uncoupled from energetic needs) and trigger learned associations between the stimulus and the reward (conditioning).”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationInterventions that decrease BMI and reduce plasma insulin and leptin enhance sensitivity to psychostimulant drugs.
“Moreover, interventions that decrease BMI and reduce plasma levels of insulin and leptin enhance the sensitivity to psychostimulant drugs (25),”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25] Davis, 2010, Insulin, leptin and reward, Trends Endocrinol Metab source
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Classified as probably not a substantial claim.
InterpretationcitationBlunted DA activation by consumption of drug or food could trigger overconsumption to compensate for the blunted reward circuit response.
“Since this is not what is seen in the clinic, it was suggested that blunted DA activation by consumption (of drug or food) could trigger overconsumption to compensate for the blunted response of the reward circuit (46).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [46] Stice, 2008, Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele, Science source
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PremisecitationIn humans, ingestion of palatable food releases DA in striatum in proportion to meal pleasantness ratings and activates reward circuitry.
“In humans, the ingestion of palatable food releases DA in the striatum in proportion to the ratings of meal pleasantness (42) and activates reward circuitry (43).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [42] Small, 2003, Feeding-induced dopamine release in dorsal striatum correlates with meal pleasantness ratings in healthy human volunteers, Neuroimage source
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- cites [43] Volkow, 2008, Overlapping neuronal circuits in addiction and obesity: Evidence of systems pathology, Philos Trans R Soc Lond B Biol Sci source
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PremisecitationCertain foods, especially those rich in sugars and fat, are potently rewarding and can trigger addictive-like behaviors in laboratory animals and humans.
“Certain foods, particularly those rich in sugars and fat, are also potently rewarding (40) and can trigger addictive like behaviors in laboratory animals (41) and humans (27).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [40] Lenoir, 2007, Intense sweetness surpasses cocaine reward, PLoS One source
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- cites [41] Avena, 2008, Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake, Neurosci Biobehav Rev source
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- cites [27] Volkow, 2007, Issues for DSM-V: Should obesity be included as a brain disorder?, Am J Psychiatry source
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PremisereasoningBrain DA pathways play central roles in obesity and addiction.
“Brain DA pathways, which modulate the behavioral responses to environmental stimuli, play central roles in obesity (also in addiction).”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationIn striatum, D2 receptors mediate indirect pathway signaling to frontocortical regions; down-regulation enhances drug sensitization, while upregulation interferes with drug consumption.
“In the striatum, D2 receptors mediate signaling through the indirect pathway that modulates frontocortical regions, and its down-regulation enhances drug sensitization in animal models (74), whereas its upregulation interferes with drug consumption (75).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [74] Ferguson, 2011, Transient neuronal inhibition reveals opposing roles of indirect and direct pathways in sensitization, Nat Neurosci source
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- cites [75] Thanos, 2008, D2R DNA transfer into the nucleus accumbens attenuates cocaine self-administration in rats, Synapse source
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PremisecitationStress is associated with increased consumption of palatable foods, weight gain, and potentiated OFC activation to food rewards.
“Still, stress is associated with increased consumption of palatable foods and weight gain and a potentiated OFC activation to food rewards (57).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [57] Rudenga, 2012, Acute stress potentiates brain response to milkshake as a function of body weight and chronic stress [published online ahead of print March 20], Int J Obes (Lond)
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PremisecitationCocaine-addicted subjects who successfully inhibited craving during drug cues decreased metabolism in medial OFC and NAc, consistent with OFC, ACC, and striatum involvement in enhanced motivation to procure drug.
“Also, when cocaine-addicted subjects purposefully inhibited craving when exposed to drug cues, those who were successful decreased metabolism in medial OFC (processes motivational value of a reinforcer) and NAc (predicts reward) (55), consistent with the involvement of OFC, ACC, and striatum in the enhanced motivation to procure the drug seen in addiction.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Volkow, 2009, Cognitive control of drug craving inhibits brain reward regions in cocaine abusers, Neuroimage source
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PremisecitationDA modulates motivation and persistence.
“Indeed, DA also modulates motivation and persistence (58).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [58] Salamone, 2007, Effort-related functions of nucleus accumbens dopamine and associated forebrain circuits, Psychopharmacology (Berl) source
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PremisecitationResearch supports a functional link between OFC impairment and disordered eating, including an association between disinhibited eating in obese adolescents and reduced OFC volume.
“Indeed, several lines of research support a functional link between OFC impairment and disordered eating, including the reported association between disinhibited eating in obese adolescents and reduced OFC volume (66).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [66] Maayan, 2011, Disinhibited eating in obese adolescents is associated with orbitofrontal volume reductions and executive dysfunction, Obesity (Silver Spring) source
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Premisenone givenDA activation of striatum by cues is involved in desire (wanting) and triggers behaviors toward consuming the desired reward.
“It appears as if DA activation of the striatum by cues (including drug-related contexts) is involved with the desire (wanting), as the trigger of behaviors geared toward consuming the desired reward.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationEvidence indicates the OFC supports conditioned cue-elicited feeding and contributes to overeating irrespective of hunger signals.
“There is evidence that the OFC also supports conditioned cue-elicited feeding (64) and that it contributes to overeating, irrespective of hunger signals (65).”
Quote in the paperSubstantial claim0 of 2 sources checkedClassified as probably not a substantial claim. May combine two claims.
InterpretationcitationPre-existing prefrontal dysfunction could underlie vulnerability to excessive drug or food consumption, exacerbated by decreases in striatal D2R.
“Similarly, a pre-existing dysfunction of prefrontal regions could also underlie the vulnerability for excessive drug or food consumption, which would be further exacerbated by decreases in striatal D2R (either drug- or stress-induced; it is unclear whether obesogenic diets decrease striatal D2R).”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationInhibition of striatal D2R or activation of D1 receptor-expressing striatal neurons enhances sensitivity to drug rewards.
“Moreover, inhibition of striatal D2R or activation of D1 receptor-expressing striatal neurons (mediate signaling in the striatal direct pathway) enhances the sensitivity to drug rewards (74).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [74] Ferguson, 2011, Transient neuronal inhibition reveals opposing roles of indirect and direct pathways in sensitization, Nat Neurosci source
Not checked in the free run.
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PremisecitationDysregulation of striatal D2R signaling has been implicated in obesity and compulsive food intake in obese rodents.
“Dysregulation of striatal D2R signaling has also been implicated in obesity (76,77) and in compulsive food intake in obese rodents (78).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [76] de Weijer, 2011, Lower striatal dopamine D2/3 receptor availability in obese compared with non-obese subjects, EJNMMI Res source
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- cites [77] Geiger, 2009, Deficits of mesolimbic dopamine neurotransmission in rat dietary obesity, Neuroscience source
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- cites [78] Johnson, 2010, Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats, Nat Neurosci source
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PremisecitationWhen nonobese male subjects inhibited food craving during food cues, they decreased activity in amygdala, OFC, hippocampus, insula, and striatum; OFC decreases were associated with reduced food craving.
“Indeed, imaging studies showed that when nonobese male subjects were asked to inhibit their craving for food when exposed to food cues, they decreased activity in amygdala, OFC, hippocampus, insula, and striatum; and OFC decreases were associated with reductions in food craving (54).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [54] Wang, 2009, Evidence of gender differences in the ability to inhibit brain activation elicited by food stimulation, Proc Natl Acad Sci U S A source
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InterpretationreasoningBecause OFC and ACC impairments are associated with compulsive behaviors and impulsivity, impaired dopamine modulation in these regions likely contributes to compulsive and impulsive drug or food intake.
“In addition, because impairments in OFC and ACC are associated with compulsive behaviors and impulsivity, impaired modulation of dopamine in these regions is likely to contribute to the compulsive and impulsive patterns of drug (addiction) or food (obesity) intake.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationVentral and medial prefrontal regions including OFC and ventral ACC become activated with exposure to craving-inducing drug stimuli or cues, in contrast to decreases in prefrontal activity in detoxified cocaine abusers not stimulated by drug cues.
“In contrast to the decreases in prefrontal activity reported in detoxified cocaine abusers when not stimulated with drug or drug cues [see review (59)], ventral and medial prefrontal regions (including OFC and ventral ACC) become activated with exposure to craving-inducing stimuli (either drugs or cues) (60,61).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [59] Volkow, 2009, Imaging dopamine's role in drug abuse and addiction, Neuropharmacology source
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- cites [60] Grant, 1996, Activation of memory circuits during cue-elicited cocaine craving, Proc Natl Acad Sci U S A source
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- cites [61] Wang, 1999, Regional brain metabolic activation during craving elicited by recall of previous drug experiences, Life Sci source
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InterpretationreasoningIn addiction, drug taking becomes the main motivational drive, so addicted subjects are aroused by obtaining drug but withdrawn and apathetic to non-drug activities.
“Because drug taking becomes the main motivational drive in addiction, addicted subjects are aroused and motivated by the process of obtaining the drug but withdrawn and apathetic when exposed to non–drug-related activities.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationGreater medial OFC volumes are seen in bulimia nervosa and binge-eating disorder patients, and OFC damage in rhesus monkeys results in hyperphagia.
“In contrast, greater volumes of the medial OFC were seen in both bulimia nervosa and binge-eating disorder patients (67), and damage to the OFC in rhesus monkeys has been reported to result in hyperphagia (68).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [67] Schafer, 2010, Regional grey matter volume abnormalities in bulimia nervosa and binge-eating disorder, Neuroimage source
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- cites [68] Machado, 2007, Measuring reward assessment in a semi-naturalistic context: The effects of selective amygdala, orbital frontal or hippocampal lesions, Neuroscience source
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PremisecitationThe OFC is involved in attributing salience value to food and assessing expected pleasantness and palatability based on context.
“The OFC is similarly involved in attributing salience value to food (62), helping to assess its expected pleasantness and palatability as a function of its context.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [62] Grabenhorst, 2008, How cognition modulates affective responses to taste and flavor: Top-down influences on the orbitofrontal and pregenual cingulate cortices, Cereb Cortex source
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PremisecitationReduced availability of striatal D2R receptors is a consistent abnormality across many drug addictions and can persist months after detoxification.
“Imaging studies revealed that reduced availability of striatal D2R receptors is a consistent abnormality across a wide variety of drug addictions and one that can persist months after detoxification [reviewed in (59)].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [59] Volkow, 2009, Imaging dopamine's role in drug abuse and addiction, Neuropharmacology source
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Premisenone givenThe insula is a primary gustatory area participating in eating behaviors such as taste.
“The insula is also a primary gustatory area, which participates in many aspects of eating behaviors, such as taste.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationSubjects recovered from anorexia nervosa show less insular activation when tasting sucrose and no association of pleasantness with insular activation as controls do.
“In contrast, subjects who have recovered from anorexia nervosa show less insular activation when tasting sucrose and no association of feelings of pleasantness with insular activation as observed in control subjects (104).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [104] Wagner, 2008, Altered insula response to taste stimuli in individuals recovered from restricting-type anorexia nervosa, Neuropsychopharmacology source
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PremisecitationThe insula, especially anterior regions, is reciprocally connected to limbic regions and supports interoceptive functions, integrating autonomic/visceral information with emotion and motivation and providing conscious awareness of urges.
“The insula, particularly its more anterior regions, is reciprocally connected to several limbic regions and supports interoceptive functions, integrating the autonomic and visceral information with emotion and motivation and providing conscious awareness of these urges (95).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [95] Naqvi, 2009, The hidden island of addiction: The insula, Trends Neurosci source
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationA similar transition from pleasurable to compulsive eating may occur in food addiction after exposure to obesogenic foods.
“More recently, Parylak et al. (106) have proposed that a similar transition may occur in food addiction with exposure to obesogenic foods.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [106] Parylak, 2011, The dark side of food addiction, Physiol Behav source
Not checked in the free run.
May combine two claims.
PremisecitationOther studies found significant decreases in prefrontal cortex blood flow associated with higher weight in healthy controls, and an fMRI study reported impaired executive function in obese women.
“Other studies found significant decreases in blood flow in the prefrontal cortex associated with higher weight in healthy control subjects (84,85), and a functional magnetic resonance imaging study reported impaired executive function in obese women (86).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [84] Willeumier, 2012, Elevated body mass in National Football League players linked to cognitive impairment and decreased prefrontal cortex and temporal pole activity, Transl Psychiatry source
Not checked in the free run.
- cites [85] Willeumier, 2011, Elevated BMI is associated with decreased blood flow in the prefrontal cortex using SPECT imaging in healthy adults, Obesity (Silver Spring) source
Not checked in the free run.
- cites [86] Kishinevsky, 2012, fMRI reactivity on a delay discounting task predicts weight gain in obese women, Appetite source
Not checked in the free run.
May combine two claims.
PremisecitationAn MRI study of elderly women found negative correlation between BMI and gray matter volumes including frontal regions, which in OFC correlated with impaired executive function.
“For example, a magnetic resonance imaging study of elderly women found a negative correlation between BMI and gray matter volumes (including frontal regions), which, in the OFC, correlated with impaired executive function (83).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [83] Walther, 2010, Structural brain differences and cognitive functioning related to body mass index in older females, Hum Brain Mapp source
Not checked in the free run.
May combine two claims.
PremisecitationWhen normal weight women tasted sucrose, both insula and DA midbrain areas activated, whereas sucralose only activated the insula.
“For example, when normal weight women tasted a sweetener with calories (sucrose), both the insula and DA midbrain areas became activated, whereas tasting a calorie-free sweetener (sucralose) only activated the insula (103).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [103] Frank, 2008, Sucrose activates human taste pathways differently from artificial sweetener, Neuroimage source
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationThe dark side of addiction is a transition from initial pleasurable drug use to compulsive drug consumption aimed at relieving negative emotional states.
“The dark side of addiction was initially proposed by Koob and Le Moal (105) to describe the transition that drug-addicted individuals experience between the initial, pleasurable use of drugs to the one that, with repeated use, results in drug consumption to relieve negative emotional states.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [105] Koob, 2005, Plasticity of reward neurocircuitry and the 'dark side' of drug addiction, Nat Neurosci source
Not checked in the free run.
May combine two claims.
PremisecitationNeurons in the rostromedial tegmental nucleus receive major input from the lateral habenula, project to VTA dopamine neurons, and are activated after food deprivation.
“The habenula is also implicated in food reward: neurons in the rostromedial tegmental nucleus, which receive a major input from the lateral habenula, project to VTA DA neurons and are activated after food deprivation (110).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [110] Jhou, 2009, The rostromedial tegmental nucleus (RMTg), a GABAergic afferent to midbrain dopamine neurons, encodes aversive stimuli and inhibits motor responses, Neuron source
Not checked in the free run.
Classified as probably not a substantial claim. May combine two claims.
PremisecitationCentral to that model is enhanced sensitivity of the extended amygdala and increased signaling through corticotropin-releasing factor and related peptides, which mediate stress responses.
“Central to their model is an enhanced sensitivity of the extended amygdala and increased signaling through corticotropin-releasing factor and corticotropin-releasing factor related peptides, which mediate responses to stress.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [106] Parylak, 2011, The dark side of food addiction, Physiol Behav source
Not checked in the free run.
Probably not a substantial claim: may not pass S2 (checkable).
InterpretationreasoningThis model helps explain the many contact points between obesity and addiction.
“This model helps explain the proliferating examples of contact points between obesity and addiction, some of which were highlighted in this review.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S4 (based). May combine two claims.
Interpretationnone givenSmoking and obesity, the two largest preventable threats to public health, involve the reward circuit that drives individuals to consume rewards despite their harm to health.
“It is telling that the two largest preventable threats to public health (smoking and obesity) involve the reward circuit that drives the motivation of individuals to consume rewards despite the fact that they are harmful to their health.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningEnhanced habenula sensitivity resulting from chronic drug exposure could cause greater reactivity to drug cues and contribute to dysphoric states during withdrawal.
“Thus, an enhanced sensitivity of the habenula, as a result of chronic drug exposure, could underlie a greater reactivity to drug cues and also contribute to dysphoric states during withdrawal.”
Quote in the paperSubstantial claim
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
A less responsive dopamine system leads to a greater propensity towards obesity, similar to other addictive disorders.
“Similar to other addictive disorders in which perturbations in brain regions within the core and extended reward networks have been reported, a less responsive dopamine system leads to a greater propensity towards obesity 40, 85, 86, 87, 88.”
From History of early life adversity is associated with increased food addiction and sex-specific alterations in reward network connectivity in obesity (2019) · cites this paper as [86]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Cited study does not match the described preclinical finding
MinorThe text cites reference 47 for a preclinical finding about decreased VTA dopamine activity and increased food consumption. Reference 47 is titled as a study of reward-system activation in obese women viewing food pictures, not a preclinical study of dopamine activity or consumption.
“Preclinical studies showing that decreased DA activity in VTA results in a dramatic increase in the consumption of high-fat foods (47) partially support this hypothesis.”
“47. Stoeckel LE Weller RE Cook EW 3rd Twieg DB Knowlton RC Cox JE 2008 Widespread reward-system activation in obese women in response to pictures of high-calorie foods Neuroimage 41 636 647 18413289”
Cites
Predictive reward signal of dopamine neurons
Schultz, W. (1998) · Journal of Neurophysiology · doi:10.1152/jn.1998.80.1.1 · Cited by 4,564 · see citing works
Psychopharmacology: The Fourth Generation of Progress
Bloom, F. E., & Kupfer, D. J. (1995) · Medical Entomology and Zoology · Cited by 2,985 · see citing works
Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index
MAGIC, Speliotes, E. K., on behalf of Procardis Consortium, Willer, C. J., Berndt, S. I., Monda, K. L., Thorleifsson, G., Jackson, A. U., Allen, H. L., Lindgren, C. M., et al. (2010) · Nature Genetics · doi:10.1038/ng.686 · Cited by 2,912 · see citing works
Interoception: the sense of the physiological condition of the body
(Bud) Craig, A. (2003) · Current Opinion in Neurobiology · doi:10.1016/s0959-4388(03)00090-4 · Cited by 2,556 · see citing works
Haber, S. N., Fudge, J. L., & McFarland, N. R. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-06-02369.2000 · Cited by 1,610 · see citing works
Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats
Johnson, P. M., & Kenny, P. J. (2010) · Nature Neuroscience · doi:10.1038/nn.2519 · Cited by 1,495 · see citing works
Reward, dopamine and the control of food intake: implications for obesity
Volkow, N. D., Wang, G.-J., & Baler, R. D. (2011) · Trends in Cognitive Sciences · doi:10.1016/j.tics.2010.11.001 · Cited by 1,400 · see citing works
Self-citationSynaptic plasticity and addiction
Kauer, J. A., & Malenka, R. C. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2234 · Cited by 1,397 · see citing works
Avena, N. M., Rada, P., & Hoebel, B. G. (2008) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2007.04.019 · Cited by 1,358 · see citing works
Association between obesity and psychiatric disorders in the US adult population
Simon, G. E., Von Korff, M., Saunders, K., Miglioretti, D. L., Crane, P. K., van Belle, G., & Kessler, R. C. (2006) · Archives of General Psychiatry · doi:10.1001/archpsyc.63.7.824 · Cited by 1,338 · see citing works
Damage to the insula disrupts addiction to cigarette smoking
Naqvi, N. H., Rudrauf, D., Damasio, H., & Bechara, A. (2007) · Science · doi:10.1126/science.1135926 · Cited by 1,245 · see citing works
Addiction, a disease of compulsion and drive: involvement of the orbitofrontal cortex
Volkow, N. D. (2000) · Cerebral Cortex · doi:10.1093/cercor/10.3.318 · Cited by 1,240 · see citing works
Self-citationCocaine cues and dopamine in dorsal striatum: mechanism of craving in cocaine addiction
Volkow, N. D., Wang, G.-J., Telang, F., Fowler, J. S., Logan, J., Childress, A.-R., Jayne, M., Ma, Y., & Wong, C. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.1544-06.2006 · Cited by 1,164 · see citing works
Self-citationPsychopharmacology: The Fourth Generation of Progress
Green, A. I. (1996) · Psychiatric Services · doi:10.1176/ps.47.3.312 · Cited by 1,151 · see citing works
Effort-related functions of nucleus accumbens dopamine and associated forebrain circuits
Salamone, J. D., Correa, M., Farrar, A., & Mingote, S. M. (2007) · Psychopharmacology · doi:10.1007/s00213-006-0668-9 · Cited by 1,000 · see citing works
Imaging dopamine's role in drug abuse and addiction
Volkow, N. D., Fowler, J. S., Wang, G. J., Baler, R., & Telang, F. (2009) · Neuropharmacology · doi:10.1016/j.neuropharm.2008.05.022 · Cited by 988 · see citing works
Self-citationAbizaid, A., Liu, Z.-W., Andrews, Z. B., Shanabrough, M., Borok, E., Elsworth, J. D., Roth, R. H., Sleeman, M. W., Picciotto, M. R., Tschöp, M. H., et al. (2006) · Journal of Clinical Investigation · doi:10.1172/jci29867 · Cited by 984 · see citing works
Everitt, B. J., Belin, D., Economidou, D., Pelloux, Y., Dalley, J. W., & Robbins, T. W. (2008) · Philosophical Transactions of the Royal Society B: Biological Sciences · doi:10.1098/rstb.2008.0089 · Cited by 974 · see citing works
Plasticity of reward neurocircuitry and the ‘dark side’ of drug addiction
Koob, G. F., & Le Moal, M. (2005) · Nature Neuroscience · doi:10.1038/nn1105-1442 · Cited by 963 · see citing works
Activation of memory circuits during cue-elicited cocaine craving.
Grant, S., London, E. D., Newlin, D. B., Villemagne, V. L., Liu, X., Contoreggi, C., Phillips, R. L., Kimes, A. S., & Margolin, A. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.21.12040 · Cited by 936 · see citing works
Volkow, N. D., Fowler, J. S., Wang, G., Hitzemann, R., Logan, J., Schlyer, D. J., Dewey, S. L., & Wolf, A. P. (1993) · Synapse · doi:10.1002/syn.890140210 · Cited by 924 · see citing works
Self-citationVolkow, N. D., Chang, L., Wang, G.-J., Fowler, J. S., Ding, Y.-S., Sedler, M., Logan, J., Franceschi, D., Gatley, J., Hitzemann, R., et al. (2001) · American Journal of Psychiatry · doi:10.1176/appi.ajp.158.12.2015 · Cited by 916 · see citing works
Self-citationWidespread reward-system activation in obese women in response to pictures of high-calorie foods
Stoeckel, L. E., Weller, R. E., Cook, E. W., Twieg, D. B., Knowlton, R. C., & Cox, J. E. (2008) · NeuroImage · doi:10.1016/j.neuroimage.2008.02.031 · Cited by 857 · see citing works
The hidden island of addiction: the insula
Naqvi, N. H., & Bechara, A. (2009) · Trends in Neurosciences · doi:10.1016/j.tins.2008.09.009 · Cited by 833 · cited 2× · see citing works
“The insula, particularly its more anterior regions, is reciprocally connected to several limbic regions and supports interoceptive functions, integrating the autonomic and visceral information with emotion and motivation and providing conscious awareness of these urges (95).”
BackgroundResultOverlapping neuronal circuits in addiction and obesity: evidence of systems pathology
Volkow, N. D., Wang, G.-J., Fowler, J. S., & Telang, F. (2008) · Philosophical Transactions of the Royal Society B: Biological Sciences · doi:10.1098/rstb.2008.0107 · Cited by 809 · see citing works
Self-citationObesity and addiction: Neurobiological overlaps
Volkow, N. D., Wang, G. ‐., Tomasi, D., & Baler, R. D. (2013) · Obesity Reviews · doi:10.1111/j.1467-789x.2012.01031.x · Cited by 800 · see citing works
Self-citationStice, E., Spoor, S., Bohon, C., & Small, D. M. (2008) · Science · doi:10.1126/science.1161550 · Cited by 786 · see citing works
Stice, E., Spoor, S., Bohon, C., Veldhuizen, M. G., & Small, D. M. (2008) · Journal of Abnormal Psychology · doi:10.1037/a0013600 · Cited by 779 · see citing works
Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index
Speliotes, E. K., Willer, C. J., Berndt, S. I., Monda, K. L., Þorleifsson, G., Jackson, A., Allen, H. L., Lindgren, C. M., Luan, J., Mägi, R., et al. (2010) · Carolina Digital Repository (University of North Carolina at Chapel Hill) · doi:10.17615/d3bn-7g86 · Cited by 767 · see citing works
Jhou, T. C., Fields, H. L., Baxter, M. G., Saper, C. B., & Holland, P. C. (2009) · Neuron · doi:10.1016/j.neuron.2009.02.001 · Cited by 696 · see citing works
Images of desire: food-craving activation during fMRI
Pelchat, M. L., Johnson, A., Chan, R., Valdez, J., & Ragland, J. D. (2004) · NeuroImage · doi:10.1016/j.neuroimage.2004.08.023 · Cited by 667 · see citing works
Small, D. M., Jones-Gotman, M., & Dagher, A. (2003) · NeuroImage · doi:10.1016/s1053-8119(03)00253-2 · Cited by 632 · see citing works
Intense Sweetness Surpasses Cocaine Reward
Lenoir, M., Serre, F., Cantin, L., & Ahmed, S. H. (2007) · PLoS ONE · doi:10.1371/journal.pone.0000698 · Cited by 608 · see citing works
Volkow, N. D., Wang, G.-J., Telang, F., Fowler, J. S., Thanos, P. K., Logan, J., Alexoff, D., Ding, Y.-S., Wong, C., Ma, Y., et al. (2008) · NeuroImage · doi:10.1016/j.neuroimage.2008.06.002 · Cited by 573 · see citing works
Self-citationAbnormal Brain Structure Implicated in Stimulant Drug Addiction
Ersche, K. D., Jones, P. S., Williams, G. B., Turton, A. J., Robbins, T. W., & Bullmore, E. T. (2012) · Science · doi:10.1126/science.1214463 · Cited by 546 · see citing works
Volkow, N. D., Wang, G., Fowler, J. S., Tomasi, D., Telang, F., & Baler, R. (2010) · BioEssays · doi:10.1002/bies.201000042 · Cited by 532 · see citing works
Self-citationAlhadeff, A. L., Rupprecht, L. E., & Hayes, M. R. (2012) · Endocrinology · doi:10.1210/en.2011-1443 · Cited by 515 · see citing works
Neural systems and cue-induced cocaine craving
Bonson, K. (2002) · Neuropsychopharmacology · doi:10.1016/s0893-133x(01)00371-2 · Cited by 507 · see citing works
Fadel, J. R., & Deutch, A. Y. (2002) · Neuroscience · doi:10.1016/s0306-4522(02)00017-9 · Cited by 503 · see citing works
Volkow, N. D., Wang, G.-J., Telang, F., Fowler, J. S., Logan, J., Jayne, M., Ma, Y., Pradhan, K., & Wong, C. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.3371-07.2007 · Cited by 494 · see citing works
Self-citationFiglewicz, D. P., Evans, S. B., Murphy, J., Hoen, M., & Baskin, D. G. (2003) · Brain Research · doi:10.1016/s0006-8993(02)04087-8 · Cited by 482 · see citing works
PET imaging of dopamine D2 receptors during chronic cocaine self-administration in monkeys
Nader, M. A., Morgan, D., Gage, H. D., Nader, S. H., Calhoun, T. L., Buchheimer, N., Ehrenkaufer, R., & Mach, R. H. (2006) · Nature Neuroscience · doi:10.1038/nn1737 · Cited by 481 · see citing works
Bow ties, metabolism and disease
Csete, M., & Doyle, J. (2004) · Trends in biotechnology · doi:10.1016/j.tibtech.2004.07.007 · Cited by 468 · see citing works
Volkow, N. D., Wang, G., Fowler, J. S., Logan, J., Jayne, M., Franceschi, D., Wong, C., Gatley, S. J., Gifford, A. N., Ding, Y., et al. (2002) · Synapse · doi:10.1002/syn.10075 · Cited by 452 · see citing works
Self-citationJerlhag, E., Egecioglu, E., Dickson, S. L., Douhan, A., Svensson, L., & Engel, J. A. (2007) · Addiction Biology · doi:10.1111/j.1369-1600.2006.00041.x · Cited by 431 · see citing works
Ferguson, S. M., Eskenazi, D., Ishikawa, M., Wanat, M. J., Phillips, P. E. M., Dong, Y., Roth, B. L., & Neumaier, J. F. (2011) · Nature Neuroscience · doi:10.1038/nn.2703 · Cited by 418 · see citing works
Janes, A. C., Pizzagalli, D. A., Richardt, S., Frederick, B. D., Chuzi, S., Pachas, G., Culhane, M. A., Holmes, A. J., Fava, M., Evins, A. E., et al. (2010) · Biological Psychiatry · doi:10.1016/j.biopsych.2009.12.034 · Cited by 416 · see citing works
Deficits of mesolimbic dopamine neurotransmission in rat dietary obesity
Geiger, B. M., Haburcak, M., Avena, N. M., Moyer, M. C., Hoebel, B. G., & Pothos, E. N. (2009) · Neuroscience · doi:10.1016/j.neuroscience.2009.02.007 · Cited by 403 · see citing works
Exposure to appetitive food stimuli markedly activates the human brain
Wang, G.-J., Volkow, N. D., Telang, F., Jayne, M., Ma, J., Rao, M., Zhu, W., Wong, C. T., Pappas, N. R., Geliebter, A., et al. (2004) · NeuroImage · doi:10.1016/j.neuroimage.2003.11.026 · Cited by 402 · see citing works
Self-citationInvolvement of the dorsal striatum in cue-controlled cocaine seeking
Vanderschuren, L. J. M. J., Di Ciano, P., & Everitt, B. J. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.0925-05.2005 · Cited by 393 · see citing works
Palmiter, R. D. (2008) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1417.003 · Cited by 375 · see citing works
Maayan, L., Hoogendoorn, C., Sweat, V., & Convit, A. (2011) · Obesity · doi:10.1038/oby.2011.15 · Cited by 345 · see citing works
Inverse Association Between BMI and Prefrontal Metabolic Activity in Healthy Adults
Volkow, N. D., Wang, G., Telang, F., Fowler, J. S., Goldstein, R. Z., Alia‐Klein, N., Logan, J., Wong, C., Thanos, P. K., Ma, Y., et al. (2009) · Obesity · doi:10.1038/oby.2008.469 · Cited by 344 · see citing works
Self-citationGrabenhorst, F., Rolls, E. T., & Bilderbeck, A. (2008) · Cerebral Cortex · doi:10.1093/cercor/bhm185 · Cited by 337 · see citing works
Regional brain metabolic activation during craving elicited by recall of previous drug experiences
Wang, G.-J., Volkow, N. D., Fowler, J. S., Cervany, P., Hitzemann, R. J., Pappas, N. R., Wong, C. T., & Felder, C. (1999) · Life Sciences · doi:10.1016/s0024-3205(98)00619-5 · Cited by 336 · see citing works
Self-citationDavis, C. A., Levitan, R. D., Reid, C., Carter, J. C., Kaplan, A. S., Patte, K. A., King, N., Curtis, C., & Kennedy, J. L. (2009) · Obesity · doi:10.1038/oby.2009.52 · Cited by 314 · see citing works
Enhanced Striatal Dopamine Release During Food Stimulation in Binge Eating Disorder
Wang, G., Geliebter, A., Volkow, N. D., Telang, F. W., Logan, J., Jayne, M. C., Galanti, K., Selig, P. A., Han, H., Zhu, W., et al. (2011) · Obesity · doi:10.1038/oby.2011.27 · Cited by 313 · see citing works
Self-citationRinaman, L. (2010) · Brain Research · doi:10.1016/j.brainres.2010.03.059 · Cited by 311 · see citing works
Davis, J. F., Tracy, A. L., Schurdak, J. D., Tschöp, M. H., Lipton, J. W., Clegg, D. J., & Benoit, S. C. (2008) · Behavioral Neuroscience · doi:10.1037/a0013111 · Cited by 307 · see citing works
Gastric distention activates satiety circuitry in the human brain
Wang, G.-J., Tomasi, D., Backus, W., Wang, R., Telang, F., Geliebter, A., Korner, J., Bauman, A., Fowler, J. S., Thanos, P. K., et al. (2008) · NeuroImage · doi:10.1016/j.neuroimage.2007.11.008 · Cited by 297 · see citing works
Self-citationStructural brain differences and cognitive functioning related to body mass index in older females
Walther, K., Birdsill, A. C., Glisky, E. L., & Ryan, L. (2010) · Human Brain Mapping · doi:10.1002/hbm.20916 · Cited by 290 · see citing works
Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
Volkow, N. D., Fowler, J. S., Wang, G.-J., Telang, F., Logan, J., Jayne, M., Ma, Y., Pradhan, K., Wong, C., & Swanson, J. M. (2010) · NeuroImage · doi:10.1016/j.neuroimage.2009.10.088 · Cited by 283 · see citing works
Self-citationSucrose activates human taste pathways differently from artificial sweetener
Frank, G. K. W., Oberndorfer, T. A., Simmons, A. N., Paulus, M. P., Fudge, J. L., Yang, T. T., & Kaye, W. H. (2008) · NeuroImage · doi:10.1016/j.neuroimage.2007.10.061 · Cited by 274 · see citing works
Issues for DSM-V: Should obesity be included as a brain disorder?
Volkow, N. D., & O’Brien, C. P. (2007) · American Journal of Psychiatry · doi:10.1176/ajp.2007.164.5.708 · Cited by 271 · see citing works
Self-citationWagner, A., Aizenstein, H., Mazurkewicz, L., Fudge, J., Frank, G. K., Putnam, K., Bailer, U. F., Fischer, L., & Kaye, W. H. (2008) · Neuropsychopharmacology · doi:10.1038/sj.npp.1301443 · Cited by 261 · see citing works
The dark side of food addiction
Parylak, S. L., Koob, G. F., & Zorrilla, E. P. (2011) · Physiology & Behavior · doi:10.1016/j.physbeh.2011.04.063 · Cited by 257 · see citing works
Neural substrates of abstinence-induced cigarette cravings in chronic smokers
Wang, Z., Faith, M., Patterson, F., Tang, K., Kerrin, K., Wileyto, E. P., Detre, J. A., & Lerman, C. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.2966-07.2007 · Cited by 256 · see citing works
DelParigi, A., Chen, K., Salbe, A. D., Hill, J. O., Wing, R. R., Reiman, E. M., & Tataranni, P. A. (2007) · International Journal of Obesity · doi:10.1038/sj.ijo.0803431 · Cited by 255 · see citing works
Wang, G.-J., Volkow, N. D., Telang, F., Jayne, M., Ma, Y., Pradhan, K., Zhu, W., Wong, C. T., Thanos, P. K., Geliebter, A., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0807423106 · Cited by 242 · see citing works
Self-citationWilleumier, K. C., Taylor, D. V., & Amen, D. G. (2011) · Obesity · doi:10.1038/oby.2011.16 · Cited by 223 · see citing works
Rolls, E. (2008) · Acta Physiologica Hungarica · doi:10.1556/aphysiol.95.2008.2.1 · Cited by 214 · see citing works
fMRI reactivity on a delay discounting task predicts weight gain in obese women
Kishinevsky, F. I., Cox, J. E., Murdaugh, D. L., Stoeckel, L. E., Cook, E. W., & Weller, R. E. (2012) · Appetite · doi:10.1016/j.appet.2011.11.029 · Cited by 191 · see citing works
Gustatory reward and the nucleus accumbens
Norgren, R., Hajnal, A., & Mungarndee, S. S. (2006) · Physiology & Behavior · doi:10.1016/j.physbeh.2006.05.024 · Cited by 181 · see citing works
Lower striatal dopamine D2/3 receptor availability in obese compared with non-obese subjects
de Weijer, B. A., van de Giessen, E., van Amelsvoort, T. A., Boot, E., Braak, B., Janssen, I. M., van de Laar, A., Fliers, E., Serlie, M. J., & Booij, J. (2011) · EJNMMI Research · doi:10.1186/2191-219x-1-37 · Cited by 176 · see citing works
DelParigi, A., Chen, K., Salbe, A. D., Reiman, E. M., & Tataranni, P. A. (2005) · NeuroImage · doi:10.1016/j.neuroimage.2004.08.035 · Cited by 158 · see citing works
Blum, K., Braverman, E. R., Wood, R. C., Gill, J., Li, C., Chen, T. J. H., Taub, M., Montgomery, A. R., Sheridan, P. J., & Cull, J. G. (1996) · Pharmacogenetics · doi:10.1097/00008571-199608000-00003 · Cited by 149 · see citing works
D2R DNA transfer into the nucleus accumbens attenuates cocaine self-administration in rats
Thanos, P. K., Michaelides, M., Umegaki, H., & Volkow, N. D. (2008) · Synapse · doi:10.1002/syn.20523 · Cited by 143 · see citing works
Self-citationA neural systems analysis of the potentiation of feeding by conditioned stimuli.
Holland, P., & Petrovich, G. (2005) · Physiology and Behavior · doi:10.1016/j.physbeh.2005.08.062 · Cited by 132 · see citing works
Alcohol use disorders after bariatric surgery
Suzuki, J., Haimovici, F., & Chang, G. (2012) · Obesity Surgery · doi:10.1007/s11695-010-0346-1 · Cited by 130 · see citing works
Davis, J. F., Choi, D. L., & Benoit, S. C. (2010) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2009.08.004 · Cited by 129 · see citing works
Leshan, R. L., Opland, D. M., Louis, G. W., Leinninger, G. M., Patterson, C. M., Rhodes, C. J., Münzberg, H., & Myers, M. G. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.1001-10.2010 · Cited by 127 · see citing works
Functional implications of glutamatergic projections to the ventral tegmental area
Geisler, S., & Wise, R. A. (2008) · Reviews in the Neurosciences · doi:10.1515/revneuro.2008.19.4-5.227 · Cited by 125 · see citing works
Regional grey matter volume abnormalities in bulimia nervosa and binge-eating disorder
Schäfer, A., Vaitl, D., & Schienle, A. (2010) · NeuroImage · doi:10.1016/j.neuroimage.2009.12.063 · Cited by 122 · see citing works
Figlewicz, D. P., Bennett, J. L., Aliakbari, S., Zavosh, A., & Sipols, A. J. (2008) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.90334.2008 · Cited by 115 · see citing works
Nair, S. G., Adams-Deutsch, T., Epstein, D. H., & Shaham, Y. (2009) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2009.05.003 · Cited by 112 · see citing works
Modulation of the mesolimbic dopamine system by leptin
Opland, D. M., Leinninger, G. M., & Myers (2010) · Brain Research · doi:10.1016/j.brainres.2010.04.028 · Cited by 111 · see citing works
Body mass predicts orbitofrontal activity during visual presentations of high-calorie foods
Killgore, W. D. S., & Yurgelun-Todd, D. A. (2005) · NeuroReport · doi:10.1097/00001756-200505310-00016 · Cited by 104 · see citing works
Riggs, N. R., Spruijt-Metz, D., Chou, C.-P., & Pentz, M. A. (2012) · Child Neuropsychology · doi:10.1080/09297049.2011.555759 · Cited by 97 · see citing works
Luo, Z., Volkow, N. D., Heintz, N., Pan, Y., & Du, C. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.2369-11.2011 · Cited by 90 · see citing works
Self-citationBody Mass Index and Marijuana Use
Warren, M., Frost-Pineda, K., & Gold, M. (2005) · Journal of Addictive Diseases · doi:10.1300/j069v24n03_08 · Cited by 86 · see citing works
Reduced nicotine reward in obesity: cross-comparison in human and mouse
Blendy, J. A., Strasser, A., Walters, C. L., Perkins, K. A., Patterson, F., Berkowitz, R., & Lerman, C. (2005) · Psychopharmacology · doi:10.1007/s00213-005-2167-9 · Cited by 81 · see citing works
Ray, L. A., Barr, C. S., Blendy, J. A., Oslin, D. W., Goldman, D. A., & Anton, R. F. (2011) · Alcoholism Clinical and Experimental Research · doi:10.1111/j.1530-0277.2011.01633.x · Cited by 80 · see citing works
Taste pathways that mediate accumbens dopamine release by sapid sucrose
Hajnal, A., & Norgren, R. (2005) · Physiology & Behavior · doi:10.1016/j.physbeh.2004.12.014 · Cited by 80 · see citing works
CNR1 gene polymorphisms in addictive disorders: a systematic review and a meta-analysis
Benyamina, A., Kébir, O., Blecha, L., Reynaud, M., & Krebs, M. (2010) · Addiction Biology · doi:10.1111/j.1369-1600.2009.00198.x · Cited by 79 · see citing works
Lasseter, H. C., Wells, A. M., Xie, X., & Fuchs, R. A. (2011) · Neuropsychopharmacology · doi:10.1038/npp.2010.209 · Cited by 72 · see citing works
Brown, R. M., Short, J. L., & Lawrence, A. J. (2010) · PLoS ONE · doi:10.1371/journal.pone.0015889 · Cited by 69 · see citing works
Association of Body Mass and Brain Activation during Gastric Distention: Implications for Obesity
Tomasi, D., Wang, G.-J., Wang, R., Backus, W., Geliebter, A., Telang, F., Jayne, M. C., Wong, C., Fowler, J. S., & Volkow, N. D. (2009) · PLoS ONE · doi:10.1371/journal.pone.0006847 · Cited by 64 · see citing works
Self-citationCognitive restraint and sensitivity to cues for hunger and satiety
Ogden, J., & Wardle, J. (1990) · Physiology & Behavior · doi:10.1016/0031-9384(90)90112-h · Cited by 63 · see citing works
Executive function and latent classes of childhood obesity risk
Riggs, N. R., Huh, J., Chou, C.-P., Spruijt-Metz, D., & Pentz, M. A. (2012) · Journal of Behavioral Medicine · doi:10.1007/s10865-011-9395-8 · Cited by 57 · see citing works
Acute stress potentiates brain response to milkshake as a function of body weight and chronic stress
Rudenga, K. J., Sinha, R., & Small, D. M. (2013) · International Journal of Obesity · doi:10.1038/ijo.2012.39 · Cited by 56 · see citing works
Zhang, F., Zhou, W., Liu, H., Zhu, H., Tang, S., Lai, M., & Yang, G. (2005) · Neuroscience Letters · doi:10.1016/j.neulet.2005.06.008 · Cited by 51 · see citing works
Relationship between Substance Use and Body Mass Index in Young Males
Blüml, V., Kapusta, N., Vyssoki, B., Kogoj, D., Walter, H., & Lesch, O. M. (2012) · The American Journal on Addictions · doi:10.1111/j.1521-0391.2011.00192.x · Cited by 51 · see citing works
Central melanocortins modulate mesocorticolimbic activity and food seeking behavior in the rat
Davis, J. F., Choi, D. L., Schurdak, J. D., Krause, E. G., Fitzgerald, M. F., Lipton, J. W., Sakai, R. R., & Benoit, S. C. (2010) · Physiology & Behavior · doi:10.1016/j.physbeh.2010.12.017 · Cited by 49 · see citing works
Willeumier, K. C., Taylor, D. V., & Amen, D. (2012) · Translational Psychiatry · doi:10.1038/tp.2011.67 · Cited by 42 · see citing works
Forebrain circuits and control of feeding by learned cues
Petrovich, G. D. (2011) · Neurobiology of Learning and Memory · doi:10.1016/j.nlm.2010.10.003 · Cited by 37 · see citing works
Machado, C. J., & Bachevalier, J. (2007) · Neuroscience · doi:10.1016/j.neuroscience.2007.06.035 · Cited by 35 · see citing works
Genetic Variation and Effects on Human Eating Behavior
de Krom, M., Bauer, F., Collier, D. A., Adan, R. A. H., & la Fleur, S. E. (2009) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-080508-141124 · Cited by 34 · see citing works
Ball, K. T., Combs, T. A., & Beyer, D. N. (2011) · Behavioural Brain Research · doi:10.1016/j.bbr.2011.03.064 · Cited by 24 · see citing works
What does the habenula tell dopamine neurons?
Kimura, M., Satoh, T., & Matsumoto, N. (2007) · Nature Neuroscience · doi:10.1038/nn0607-677 · Cited by 24 · see citing works
N. Kearns, D., A. Gomez-Serrano, M., & J. Tunstall, B. (2011) · Current Drug Abuse Reviewse · doi:10.2174/1874473711104040261 · Cited by 22 · see citing works
Schleinitz, D., Carmienke, S., Böttcher, Y., Tönjes, A., Berndt, J., Klöting, N., Enigk, B., Müller, I., Dietrich, K., Breitfeld, J., et al. (2010) · Pharmacogenomics · doi:10.2217/pgs.10.42 · Cited by 18 · see citing works
Gudelsky, G. A., Passaro, E. A., & Meltzer, H. Y. (1986) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(25)38993-7 · Cited by 7 · see citing works
Volkow, N. D., Wang, G.-J., Begleiter, H., Porjesz, B., Fowler, J. S., Telang, F., Wong, C., Ma, Y., Logan, J., Goldstein, R., et al. (2006) · Archives of General Psychiatry · doi:10.1001/archpsyc.63.9.999 · Cited by 2 · see citing works
Self-citationNaukkarinen, J., Surakka, I., Pietiläinen, K. H., Rissanen, A., Salomaa, V., Ripatti, S., Yki-Järvinen, H., van Duijn, C. M., Wichmann, H.-E., Kaprio, J., et al. (2010) · PLoS Genetics · doi:10.1371/journal.pgen.1000976
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Brain Insulin Resistance at the Crossroads of Metabolic and Cognitive Disorders in Humans
Kullmann, S., Heni, M., Hallschmid, M., Fritsche, A., Preissl, H. T., & Häring, H. (2016) · Physiological Reviews · doi:10.1152/physrev.00032.2015 · Cited by 634 · see citing works
Upadhyay, J., Farr, O. M., Perakakis, N., Ghaly, W., & Mantzoros, C. S. (2017) · Medical Clinics of North America · doi:10.1016/j.mcna.2017.08.004 · Cited by 403 · see citing works
What is the evidence for “food addiction?” A systematic review
Gordon, E., Ariel-Donges, A., Bauman, V., & Merlo, L. (2018) · Nutrients · doi:10.3390/nu10040477 · Cited by 316 · see citing works
Dissecting impulsivity and its relationships to drug addictions
Jentsch, J. D., Ashenhurst, J. R., Cervantes, M. C., Groman, S. M., James, A. S., & Pennington, Z. T. (2014) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12388 · Cited by 281 · see citing works
Effects of non-invasive neurostimulation on craving: A meta-analysis
Jansen, J. M., Daams, J. G., Koeter, M. W. J., Veltman, D. J., van den Brink, W., & Goudriaan, A. E. (2013) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2013.07.009 · Cited by 284 · see citing works
Food Addiction in the Light of DSM-5
Meule, A., & Gearhardt, A. N. (2014) · Nutrients · doi:10.3390/nu6093653 · Cited by 277 · see citing works
Neuroscience of Internet Pornography Addiction: A Review and Update
Love, T., Laier, C., Brand, M., Hatch, L., & Hajela, R. (2015) · Behavioral Sciences · doi:10.3390/bs5030388 · Cited by 262 · see citing works
Brain–gut–microbiome interactions in obesity and food addiction
Gupta, A., Osadchiy, V., & Mayer, E. A. (2020) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-020-0341-5 · Cited by 268 · see citing works
NOW vs LATER brain circuits: implications for obesity and addiction
Volkow, N. D., & Baler, R. D. (2015) · Trends in Neurosciences · doi:10.1016/j.tins.2015.04.002 · Cited by 237 · see citing works
Self-citationIs Food Addictive? A Review of the Science
Gearhardt, A. N., & LaFata, E. M. (2021) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-110420-111710 · Cited by 222 · see citing works
Chuong, V., Farokhnia, M., Khom, S., Pince, C. L., Elvig, S. K., Vlkolinsky, R., Marchette, R. C. N., Koob, G. F., Roberto, M., Vendruscolo, L. F., et al. (2023) · JCI Insight · doi:10.1172/jci.insight.170671 · Cited by 214 · see citing works
Byrne, C. S., Chambers, E. S., Alhabeeb, H., Chhina, N., Morrison, D. J., Preston, T., Tedford, C., Fitzpatrick, J., Irani, C., Busza, A., et al. (2016) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.115.126706 · Cited by 201 · see citing works
Central nervous system regulation of eating: Insights from human brain imaging
Farr, O. M., Li, C. R., & Mantzoros, C. S. (2016) · Metabolism · doi:10.1016/j.metabol.2016.02.002 · Cited by 191 · see citing works
Robinson, M. J. F., Burghardt, P. R., Patterson, C. M., Nobile, C. W., Akil, H., Watson, S. J., Berridge, K. C., & Ferrario, C. R. (2015) · Neuropsychopharmacology · doi:10.1038/npp.2015.71 · Cited by 185 · see citing works
Reward processing in obesity, substance addiction and non‐substance addiction
García‐García, I., Horstmann, A., Jurado, M. Á., Garolera, M., Chaudhry, S. J., Margulies, D. S., Villringer, A., & Neumann, J. (2014) · Obesity Reviews · doi:10.1111/obr.12221 · Cited by 180 · see citing works
From Belly to Brain: Targeting the Ghrelin Receptor in Appetite and Food Intake Regulation
Howick, K., Griffin, B. T., Cryan, J. F., & Schellekens, H. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18020273 · Cited by 178 · see citing works
The Neurobiology of “Food Addiction” and Its Implications for Obesity Treatment and Policy
Carter, A., Hendrikse, J. J., Lee, N., Yücel, M., Verdejo‐García, A., Andrews, Z. B., & Hall, W. (2016) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-071715-050909 · Cited by 176 · see citing works
Song, S., Zilverstand, A., Gui, W., Li, H., & Zhou, X. (2018) · Brain stimulation · doi:10.1016/j.brs.2018.12.975 · Cited by 172 · see citing works
Self-harm Emergencies After Bariatric Surgery
Bhatti, J. A., Nathens, A. B., Thiruchelvam, D., Grantcharov, T., Goldstein, B. I., & Redelmeier, D. A. (2015) · JAMA Surgery · doi:10.1001/jamasurg.2015.3414 · Cited by 171 · see citing works
Associations Among Body Mass Index, Cortical Thickness, and Executive Function in Children
Laurent, J. S., Watts, R., Adise, S., Allgaier, N. A., Chaarani, B., Garavan, H., Potter, A., & Mackey, S. (2019) · Archives of Pediatrics and Adolescent Medicine · doi:10.1001/jamapediatrics.2019.4708 · Cited by 171 · see citing works
Neuropsychiatric Comorbidity in Obesity: Role of Inflammatory Processes
Castanon, N., Lasselin, J., & Capuron, L. (2014) · Frontiers in Endocrinology · doi:10.3389/fendo.2014.00074 · Cited by 160 · see citing works
A neuromarker for drug and food craving distinguishes drug users from non-users
Koban, L., Wager, T. D., & Hedy Kober, A. (2022) · Nature Neuroscience · doi:10.1038/s41593-022-01228-w · Cited by 150 · see citing works
Davis, C. A. (2016) · Appetite · doi:10.1016/j.appet.2016.11.001 · Cited by 155 · see citing works
Guo, J., Simmons, W. K., Herscovitch, P., Martin, A. D., & Hall, K. D. (2014) · Molecular Psychiatry · doi:10.1038/mp.2014.102 · Cited by 148 · see citing works
Nunes-Neto, P. R., Köhler, C. A., Schuch, F. B., Solmi, M., Quevedo, J., Maes, M., Murru, A., Vieta, E., McIntyre, R. S., McElroy, S. L., et al. (2018) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2017.10.003 · Cited by 150 · see citing works
Oxytocin׳s role in anxiety: A critical appraisal
MacDonald, K., & Feifel, D. (2014) · Brain Research · doi:10.1016/j.brainres.2014.01.025 · Cited by 139 · see citing works
Gender-related Differences in Food Craving and Obesity.
Hallam, J., Boswell, R. G., DeVito, E. E., & Hedy Kober, A. (2016) · PubMed Central · Cited by 142 · see citing works
Goldstone, A. P., Prechtl, C. G., Scholtz, S., Miras, A. D., Chhina, N., Durighel, G., Deliran, S. S., Beckmann, C. F., Ghatei, M. A., Ashby, D. R., et al. (2014) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.113.075291 · Cited by 140 · see citing works
Glutamatergic transmission in drug reward: implications for drug addiction
D’Souza, M. S. (2015) · Frontiers in Neuroscience · doi:10.3389/fnins.2015.00404 · Cited by 141 · see citing works
Food Addiction: Implications for the Diagnosis and Treatment of Overeating
Adams, R. C., Sedgmond, J., Maizey, L., Chambers, C., & Lawrence, N. (2019) · Nutrients · doi:10.3390/nu11092086 · Cited by 143 · see citing works
Wang, W. J., Volkow, N. D., Berger, N. A., Davis, P. B., Kaelber, D. C., & Xu, R. (2024) · Nature Communications · doi:10.1038/s41467-024-48780-6 · Cited by 138 · see citing works
Self-citationBrain functional and structural magnetic resonance imaging of obesity and weight loss interventions
Li, G., Hu, Y., Zhang, W., Wang, J., Ji, W., Manza, P., Volkow, N. D., Zhang, Y., & Wang, G. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02025-y · Cited by 135 · see citing works
Self-citationVentral and Dorsal Striatum Networks in Obesity: Link to Food Craving and Weight Gain
Contreras‐Rodríguez, O., Martín-Pérez, C., Vilar‐López, R., & Verdejo‐García, A. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.11.020 · Cited by 131 · see citing works
High Trait Impulsivity Predicts Food Addiction-Like Behavior in the Rat
Velázquez-Sánchez, C., Ferragud, A., Moore, C. F., Everitt, B. J., Sabino, V., & Cottone, P. (2014) · Neuropsychopharmacology · doi:10.1038/npp.2014.98 · Cited by 130 · see citing works
Pathological overeating: emerging evidence for a compulsivity construct
Moore, C. F., Sabino, V., Koob, G. F., & Cottone, P. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.269 · Cited by 126 · see citing works
Glucose-responsive neurons of the paraventricular thalamus control sucrose-seeking behavior
Labouèbe, G., Boutrel, B., Tarussio, D., & Thorens, B. (2016) · Nature Neuroscience · doi:10.1038/nn.4331 · Cited by 125 · see citing works
Food Addiction in Overweight and Obese Adolescents Seeking Weight‐loss Treatment
Meule, A., Hermann, T., & Kübler, A. (2015) · European Eating Disorders Review · doi:10.1002/erv.2355 · Cited by 127 · see citing works
Farokhnia, M., Grodin, E. N., Lee, M. R., Oot, E. N., Blackburn, A. N., Stangl, B. L., Schwandt, M. L., Farinelli, L. A., Momenan, R., Ramchandani, V. A., et al. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.226 · Cited by 120 · see citing works
Resting-state functional connectivity of the human hypothalamus
Kullmann, S., Heni, M., Linder, K., Zipfel, S., Häring, H., Veit, R., Fritsche, A., & Preissl, H. T. (2014) · Human Brain Mapping · doi:10.1002/hbm.22607 · Cited by 124 · see citing works
Optogenetic Central Amygdala Stimulation Intensifies and Narrows Motivation for Cocaine
Warlow, S. M., Robinson, M. J. F., & Berridge, K. C. (2017) · Journal of Neuroscience · doi:10.1523/jneurosci.3141-16.2017 · Cited by 122 · see citing works
Foods are differentially associated with subjective effect report questions of abuse liability
LaFata, E. M., Smeal, J. K., & Gearhardt, A. N. (2017) · PLoS ONE · doi:10.1371/journal.pone.0184220 · Cited by 120 · see citing works
Mechanisms of Body Weight Fluctuations in Parkinson’s Disease
Kistner, A., Lhommée, E., & Krack, P. (2014) · Frontiers in Neurology · doi:10.3389/fneur.2014.00084 · Cited by 114 · see citing works
Overlapping patterns of brain activation to food and cocaine cues in cocaine abusers
Tomasi, D. G., Wang, G., Wang, R., Caparelli, E. C., Logan, J., & Volkow, N. D. (2014) · Human Brain Mapping · doi:10.1002/hbm.22617 · Cited by 112 · see citing works
Self-citationConvergence between biological, behavioural and genetic determinants of obesity
Ghosh, S., & Bouchard, C. (2017) · Nature Reviews Genetics · doi:10.1038/nrg.2017.72 · Cited by 108 · see citing works
Domingo-Rodriguez, L., Ruiz de Azua, I., Dominguez, E., Senabre, E., Serra, I., Kummer, S., Navandar, M., Baddenhausen, S., Hofmann, C., Andero, R., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-14458-y · Cited by 109 · see citing works
Steffen, K. J., Engel, S. G., Wonderlich, J. A., Pollert, G. A., & Sondag, C. (2015) · European Eating Disorders Review · doi:10.1002/erv.2399 · Cited by 108 · see citing works
Cognitive and autonomic determinants of energy homeostasis in obesity
Richard, D. (2015) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2015.103 · Cited by 109 · see citing works
Décarie-Spain, L., Sharma, S., Hryhorczuk, C., Issa-Garcia, V., Barker, P. A., Arbour, N., Alquier, T., & Fulton, S. (2018) · Molecular Metabolism · doi:10.1016/j.molmet.2018.01.018 · Cited by 107 · see citing works
Neural Circuits for Cognitive Appetite Control in Healthy and Obese Individuals: An fMRI Study
Tuulari, J. J., Karlsson, H. K., Hirvonen, J., Salminen, P. T. P., Nuutila, P., & Nummenmaa, L. (2015) · PLoS ONE · doi:10.1371/journal.pone.0116640 · Cited by 105 · see citing works
Reiter, A. M. F., Heinze, H., Schlagenhauf, F., & Deserno, L. (2016) · Neuropsychopharmacology · doi:10.1038/npp.2016.95 · Cited by 103 · see citing works
Amylin at the interface between metabolic and neurodegenerative disorders
Lutz, T. A., & Meyer, U. (2015) · Frontiers in Neuroscience · doi:10.3389/fnins.2015.00216 · Cited by 100 · see citing works
Mies, G. W., Treur, J. L., Larsen, J. K., Halberstadt, J., Pasman, J. A., & Vink, J. M. (2017) · Appetite · doi:10.1016/j.appet.2017.08.002 · Cited by 99 · see citing works
Back By Popular Demand: A Narrative Review On The History Of Food Addiction Research
Meule, A. (2015) · PubMed Central · doi:10.5281/zenodo.48115 · Cited by 97 · see citing works
Grall‐Bronnec, M., & Sauvaget, A. (2014) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2014.10.013 · Cited by 96 · see citing works
Addiction-like Synaptic Impairments in Diet-Induced Obesity
Brown, R. M., Kupchik, Y. M., Spencer, S. M., García‐Keller, C., Spanswick, D. C., Lawrence, A. J., Simonds, S. E., Schwartz, D., Jordan, K. A., Jhou, T. C., et al. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.11.019 · Cited by 96 · see citing works
Potential psychological & neural mechanisms in binge eating disorder: Implications for treatment
Hedy Kober, A., & Boswell, R. G. (2017) · Clinical Psychology Review · doi:10.1016/j.cpr.2017.12.004 · Cited by 91 · see citing works
Janssen, L. K., Duif, I., van Loon, I., Wegman, J., de Vries, J. H. M., Cools, R., & Aarts, E. (2016) · NeuroImage · doi:10.1016/j.neuroimage.2016.11.015 · Cited by 88 · see citing works
The Trace Amine-Associated Receptor 1 Agonist RO5256390 Blocks Compulsive, Binge-like Eating in Rats
Ferragud, A., Howell, A. D., Moore, C. F., Ta, T. L., Hoener, M. C., Sabino, V., & Cottone, P. (2016) · Neuropsychopharmacology · doi:10.1038/npp.2016.233 · Cited by 84 · see citing works
Carbine, K. A., Rodeback, R. E., Modersitzki, E., Miner, M., LeCheminant, J. D., & Larson, M. J. (2018) · Appetite · doi:10.1016/j.appet.2018.05.135 · Cited by 82 · see citing works
Hume, D. J., Howells, F. M., Rauch, L., Kroff, J., & Lambert, E. V. (2014) · Appetite · doi:10.1016/j.appet.2014.11.012 · Cited by 79 · see citing works
Munn‐Chernoff, M. A., Johnson, E. C., Chou, Y., Coleman, J. R. I., Thornton, L. M., Walters, R. K., Yılmaz, Z., Baker, J. H., Hübel, C., Gordon, S. D., et al. (2020) · Addiction Biology · doi:10.1111/adb.12880 · Cited by 79 · see citing works
Caravaggio, F., Borlido, C., Hahn, M., Feng, Z., Fervaha, G., Gerretsen, P., Nakajima, S., Plitman, E., Chung, J. K., Iwata, Y., et al. (2015) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyv014 · Cited by 76 · see citing works
Reducing Ventral Tegmental Dopamine D2 Receptor Expression Selectively Boosts Incentive Motivation
de Jong, J. W., Roelofs, T. J. M., Mol, F., Hillen, A. E. J., Meijboom, K. E., Luijendijk, M. C. M., van der Eerden, H. A. M., Garner, K. M., Vanderschuren, L. J. M. J., & Adan, R. A. H. (2015) · Neuropsychopharmacology · doi:10.1038/npp.2015.60 · Cited by 77 · see citing works
Angarita, G. A., Matuskey, D., Pittman, B., Costeines, J. L., Potenza, M. N., Jastreboff, A. M., Schmidt, H. D., & Malison, R. T. (2021) · Drug and Alcohol Dependence · doi:10.1016/j.drugalcdep.2021.108614 · Cited by 75 · see citing works
Palatable Hyper-Caloric Foods Impact on Neuronal Plasticity
Morin, J., Rodríguez-Durán, L. F., Guzmán-Ramos, K. R., Perez‐Cruz, C., Ferreira, G., Díaz-Cintra, S. Y., & Pacheco‐López, G. (2017) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2017.00019 · Cited by 74 · see citing works
Dong, G., Dong, H., Wang, M., Zhang, J., Zhou, W., Du, X., & Potenza, M. N. (2021) · Communications Biology · doi:10.1038/s42003-021-02395-5 · Cited by 74 · see citing works
Aberrant mesolimbic dopamine-opiate interaction in obesity
Tuominen, L., Tuulari, J., Karlsson, H., Hirvonen, J., Helin, S., Salminen, P., Parkkola, R., Hietala, J., Nuutila, P., & Nummenmaa, L. (2015) · NeuroImage · doi:10.1016/j.neuroimage.2015.08.001 · Cited by 64 · see citing works
Navas (2017) · doi:10.1002/hbm.23407 · Cited by 71 · see citing works
Neurocognitive correlates of processing food-related stimuli in a Go/No-go paradigm
Watson, T. D., & Garvey, K. T. (2013) · Appetite · doi:10.1016/j.appet.2013.07.007 · Cited by 69 · see citing works
Song, S., Zilverstand, A., Gui, W., Pan, X.-F., & Zhou, X. (2021) · Addiction · doi:10.1111/add.15686 · Cited by 64 · see citing works
Oxytocin enhances cognitive control of food craving in women
Striepens, N., Schröter, F., Stoffel‐Wagner, B., Maier, W., Hurlemann, R., & Scheele, D. (2016) · Human Brain Mapping · doi:10.1002/hbm.23308 · Cited by 63 · see citing works
Enhanced incentive motivation in obesity-prone rats is mediated by NAc core CP-AMPARs
Derman, R. C., & Ferrario, C. R. (2017) · Neuropharmacology · doi:10.1016/j.neuropharm.2017.12.039 · Cited by 59 · see citing works
Monteleone, A. M., Marzo, V. D., Monteleone, P., Grave, R. D., Aveta, T., Ghoch, M. E., Piscitelli, F., Volpe, U., Calugi, S., & Maj, M. (2016) · European Journal of Nutrition · doi:10.1007/s00394-016-1153-9 · Cited by 62 · see citing works
Kanoski, S. E., Alhadeff, A. L., Fortin, S. M., Gilbert, J. R., & Grill, H. J. (2013) · Neuropsychopharmacology · doi:10.1038/npp.2013.235 · Cited by 61 · see citing works
Developing ‘integrative’ zebrafish models of behavioral and metabolic disorders
Nguyen, M., Yang, E., Neelkantan, N., Mikhaylova, A., Arnold, R., Poudel, M. K., Stewart, A., & Kalueff, A. V. (2013) · Behavioural Brain Research · doi:10.1016/j.bbr.2013.08.012 · Cited by 59 · see citing works
High-fat diet-induced obesity and impairment of brain neurotransmitter pool
Labban, R. S. M., Alfawaz, H., Almnaizel, A. T., Hassan, W. M., Bhat, R. S., Moubayed, N., Bjørklund, G., & El-Ansary, A. K. (2020) · Translational Neuroscience · doi:10.1515/tnsci-2020-0099 · Cited by 57 · see citing works
Neuroscience of Compulsive Eating Behavior
Moore, C. F., Sabino, V., Koob, G. F., & Cottone, P. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00469 · Cited by 56 · see citing works
Affected connectivity organization of the reward system structure in obesity
Marqués‐Iturria, I., Scholtens, L. H., Garolera, M., Pueyo, R., García‐García, I., González-Tartière, P., Segura, B., Junqué, C., Palacios, M. J. S., Vernet‐Vernet, M., et al. (2015) · NeuroImage · doi:10.1016/j.neuroimage.2015.02.012 · Cited by 55 · see citing works
Davis, C. A., Levitan, R. D., Kaplan, A. S., Kennedy, J. L., & Carter, J. C. (2014) · Frontiers in Psychology · doi:10.3389/fpsyg.2014.00403 · Cited by 54 · see citing works
Carlier, N., Marshe, V. S., Cmorejova, J., Davis, C. A., & Müller, D. J. (2015) · Current Psychiatry Reports · doi:10.1007/s11920-015-0634-5 · Cited by 54 · see citing works
Kay, K. E., Parise, E. M., Lilly, N., & Williams, D. L. (2013) · Psychopharmacology · doi:10.1007/s00213-013-3248-9 · Cited by 53 · see citing works
BMI Modulates Calorie-Dependent Dopamine Changes in Accumbens from Glucose Intake
Wang, G., Tomasi, D. G., Convit, A. J., Logan, J., Wong, C., Shumay, E., Fowler, J. S., & Volkow, N. D. (2014) · PLoS ONE · doi:10.1371/journal.pone.0101585 · Cited by 53 · see citing works
Self-citationIhssen, N., Sokunbi, M. O., Lawrence, A. D., Lawrence, N., & Linden, D. E. J. (2016) · Brain Imaging and Behavior · doi:10.1007/s11682-016-9558-x · Cited by 53 · see citing works
van der Zwaal, E. M., de Weijer, B. A., van de Giessen, E., Janssen, I. M. C., Berends, F. J., van de Laar, A. W. J. M., Ackermans, M. T., Fliers, E., la Fleur, S. E., Booij, J., et al. (2016) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2016.04.009 · Cited by 52 · see citing works
Shomaker, L. B., Berman, Z., Burke, M., Annameier, S. K., Pivarunas, B., Sánchez, N., Smith, A. D., Hendrich, S. G., Riggs, N. R., Legget, K. T., et al. (2019) · Appetite · doi:10.1016/j.appet.2019.05.022 · Cited by 51 · see citing works
Chen, R., Peng-Li, D., Turel, O., Sørensen, T. A., Bechara, A., Li, Y., & He, Q. (2018) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2018.00264 · Cited by 50 · see citing works
Baladi, M. G., Horton, R. E., Owens, W. A., Daws, L. C., & France, C. P. (2015) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyv024 · Cited by 48 · see citing works
The Effect of Obesity on the Availabilities of Dopamine and Serotonin Transporters
Nam, S. B., Keun-young Kim, A., Kim, B., Im, H., Lee, S. H., Kim, S., Kim, I. J., & Pak, K. (2018) · Scientific Reports · doi:10.1038/s41598-018-22814-8 · Cited by 49 · see citing works
Chew, N., Ng, C. H., Muthiah, M. D., & Sanyal, A. J. (2022) · Current Atherosclerosis Reports · doi:10.1007/s11883-022-01027-5 · Cited by 49 · see citing works
Do Dopaminergic Impairments Underlie Physical Inactivity in People with Obesity?
Kravitz, A. V., O’Neal, T. J., & Friend, D. M. (2016) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2016.00514 · Cited by 48 · see citing works
Brain on Fire: Incentive Salience, Hedonic Hot Spots, Dopamine, Obesity, and Other Hunger Games
Cameron, J. D., Chaput, J., Sjödin, A. M., & Goldfield, G. S. (2017) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-071816-064855 · Cited by 48 · see citing works
DIETARY INFLUENCES ON COGNITION
Reichelt, A. C., Stoeckel, L., Reagan, L. P., Winstanley, C., & Page, K. (2018) · Physiology and Behavior · doi:10.1016/j.physbeh.2018.02.052 · Cited by 34 · see citing works
del Pino-Gutiérrez, A., Jiménez-Murcia, S., Fernández-Aranda, F., Agüera, Z., Granero, R., Hakansson, A., Fagundo, A. B., Bolao, F., Valdepérez, A., Mestre-Bach, G., et al. (2017) · Journal of Behavioral Addictions · doi:10.1556/2006.6.2017.051 · Cited by 48 · see citing works
Yoder, R., MacNeela, P., Conway, R. J., & Heary, C. (2017) · Obesity Surgery · doi:10.1007/s11695-017-2936-7 · Cited by 47 · see citing works
Lowe, C. J., Staines, R. W., Manocchio, F., & Hall, P. A. (2018) · NeuroImage · doi:10.1016/j.neuroimage.2018.05.013 · Cited by 48 · see citing works
Steward, T., Miranda‐Olivos, R., Soriano‐Mas, C., & Fernández‐Aranda, F. (2019) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-019-09515-x · Cited by 46 · see citing works
Fauconnier, M., Rousselet, M., Brunault, P., Thiabaud, E., Lambert, S., Rocher, B., Challet‐Bouju, G., & Grall‐Bronnec, M. (2020) · Nutrients · doi:10.3390/nu12061897 · Cited by 47 · see citing works
Hermann, P., Gál, V., Kóbor, I., Kirwan, C. B., Kovács, P., Kitka, T., Lengyel, Z., Bálint, E., Varga, B., Csekő, C., et al. (2019) · NeuroImage: Clinical · doi:10.1016/j.nicl.2019.101803 · Cited by 46 · see citing works
Osadchiy, V., Mayer, E. A., Bhatt, R., Labus, J. S., Gao, L., Kilpatrick, L. A., Liu, C., Tillisch, K., Naliboff, B., Chang, L., et al. (2019) · Obesity Science & Practice · doi:10.1002/osp4.362 · Cited by 44 · see citing works
Current research and emerging directions in emotion-cognition interactions
Dolcos, F., Wang, L., & Mather, M. (2014) · Frontiers in Integrative Neuroscience · doi:10.3389/fnint.2014.00083 · Cited by 45 · see citing works
- Authors
- Volkow, N. D., Wang, G.-J., Tomasi, D., & Baler, R. D.
- Affiliations
- National Institutes of Health (US)
- Brookhaven National Laboratory (US)
- Corresponding author
- Volkow, Nora D.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2013-05
- Volume
- 73
- Issue
- 9
- Pages
- 811-818
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC4827347
- OpenAlex
- W1981784954
- Semantic Scholar
- 905b6cf49d1dc61cb189ca21cbc230487ef7d212
- Cited by
- 380
- References
- 114
- Citations by year
- 2026: 19 · 2025: 23 · 2024: 17 · 2023: 21 · 2022: 18 · 2021: 25 · 2020: 23 · 2019: 21 · 2018: 37 · 2017: 35 · 2016: 41 · 2015: 50 · 2014: 36 · 2013: 14
- FWCI
- 6.94
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (ZIAAA000550)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- obesity, addiction, compulsive eating, reward systems, energy homeostasis, self-control, inhibitory control, palatable food, drug addiction, neural correlates
- MeSH terms
- Compulsive Behavior, Dopamine, Eating, Homeostasis, Humans, Obesity, Reward, Behavior, Addictive, Prefrontal Cortex
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-09.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-09.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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