Enhanced Striatal Dopamine Release During Food Stimulation in Binge Eating Disorder

Medical Department, Brookhaven National Laboratory, Upton, New York, USA.
Obesity (Impact Factor: 3.73). 02/2011; 19(8):1601-1608. DOI: 10.1038/oby.2011.27
Source: PubMed


Subjects with binge eating disorder (BED) regularly consume large amounts of food in short time periods. The neurobiology of BED is poorly understood. Brain dopamine, which regulates motivation for food intake, is likely to be involved. We assessed the involvement of brain dopamine in the motivation for food consumption in binge eaters. Positron emission tomography (PET) scans with [(11)C]raclopride were done in 10 obese BED and 8 obese subjects without BED. Changes in extracellular dopamine in the striatum in response to food stimulation in food-deprived subjects were evaluated after placebo and after oral methylphenidate (MPH), a drug that blocks the dopamine reuptake transporter and thus amplifies dopamine signals. Neither the neutral stimuli (with or without MPH) nor the food stimuli when given with placebo increased extracellular dopamine. The food stimuli when given with MPH significantly increased dopamine in the caudate and putamen in the binge eaters but not in the nonbinge eaters. Dopamine increases in the caudate were significantly correlated with the binge eating scores but not with BMI. These results identify dopamine neurotransmission in the caudate as being of relevance to the neurobiology of BED. The lack of correlation between BMI and dopamine changes suggests that dopamine release per se does not predict BMI within a group of obese individuals but that it predicts binge eating.

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Available from: Wei Zhu, Oct 06, 2015
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    • "For example, abstinent methamphetamine dependent (Stim) have blunted striatal dopamine receptor availability (Volkow et al., 2001b) associated with impulsivity (Lee et al., 2009), and individuals with AUDs have reduced ventral striatal dopamine transmission (Martinez et al., 2005) associated with alcohol craving (Heinz et al., 2004). Changes in dopamine transmission in obese subjects remains unclear with reported reductions in striatal D2 receptor binding that are associated with BMI (Wang et al., 2001) as well as no difference in underlying Dopamine (DA) capacity (Davis et al., 2009) in obese with binge eating disorder (BED) but enhanced dopamine transmission at presentation of food stimulus in BED (Wang et al., 2011). We have also recently reported enhanced premature responding in BDs at elevated risk for the development of AUD (Morris et al., 2015). "
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    ABSTRACT: The ability to wait and to weigh evidence is critical to behavioural regulation. These behaviors are known as waiting and reflection impulsivity. In Study 1, we examined the effects of methylphenidate (MPH), a dopamine and norepinephrine reuptake inhibitor, on waiting and reflection impulsivity in healthy young individuals. In Study 2, we assessed the role of learning from feedback in disorders of addiction. We used the recently developed 4-Choice Serial Reaction Time task and the Beads task. Twenty-eight healthy volunteers were tested twice in a randomized double-blind placebo controlled cross-over trial with 20mg MPH. In the second study we analyzed premature responses as a function of prior feedback in disorders of addiction. Study 1: MPH was associated with greater waiting impulsivity to a cue predicting reward along with faster responding to target onset without a generalized effect on reaction time or attention. MPH influenced reflection impulsivity based on baseline impulsivity. Study 2: more premature responses occurred after premature responses in stimulant dependent subjects. We show that MPH has dissociable effects on waiting and reflection impulsivity. Chronic stimulant exposure impairs learning from prior premature responses suggesting a failure to learn that premature responding is suboptimal. These findings provide a greater mechanistic understanding of waiting impulsivity. © The Author 2015. Published by Oxford University Press on behalf of CINP.
    The International Journal of Neuropsychopharmacology 06/2015; DOI:10.1093/ijnp/pyv074 · 4.01 Impact Factor
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    • "Both BED and obese subjects have been shown to discount delayed rewards at higher rates than normal controls (Manwaring et al. 2011) and a study in females suggests that BED subjects may have greater delay discounting than obese subjects without BED (Manwaring et al. 2011). Presenting food to obese human subjects with BED has been shown to result in greater striatal dopamine release than in obese subjects without BED (Wang et al. 2011). Evidence has also suggested BED to represent an extreme neurobehavioral phenotype of obesity with more prominent impulsivity (Carnell et al. 2012). "
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    ABSTRACT: Background: Evidence suggests some overlap between the pathological use of food and drugs, yet how impulsivity compares across these different clinical disorders remains unclear. Substance use disorders are commonly characterized by elevated impulsivity, and impulsivity subtypes may show commonalities and differences in various conditions. We hypothesized that obese subjects with binge-eating disorder (BED) and abstinent alcohol-dependent cohorts would have relatively more impulsive profiles compared to obese subjects without BED. We also predicted decision impulsivity impairment in obesity with and without BED. Method: Thirty obese subjects with BED, 30 without BED and 30 abstinent alcohol-dependent subjects and age- and gender-matched controls were tested on delay discounting (preference for a smaller immediate reward over a larger delayed reward), reflection impulsivity (rapid decision making prior to evidence accumulation) and motor response inhibition (action cancellation of a prepotent response). Results: All three groups had greater delay discounting relative to healthy volunteers. Both obese subjects without BED and alcohol-dependent subjects had impaired motor response inhibition. Only obese subjects without BED had impaired integration of available information to optimize outcomes over later trials with a cost condition. Conclusions: Delay discounting appears to be a common core impairment across disorders of food and drug intake. Unexpectedly, obese subjects without BED showed greater impulsivity than obese subjects with BED. We highlight the dissociability and heterogeneity of impulsivity subtypes and add to the understanding of neurocognitive profiles across disorders involving food and drugs. Our results have therapeutic implications suggesting that disorder-specific patterns of impulsivity could be targeted.
    Psychological Medicine 08/2014; 45(04):1-12. DOI:10.1017/S0033291714001834 · 5.94 Impact Factor
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    • "However, more studies using salient reward-related cues are pertinent in patients suffering from GD. Notably, Leyton and Vezina provide evidence across several types of addictions. For example a recent study reported increased striatal dopamine responses to food stimuli in binge eaters (Wang et al., 2011). Although electrophysiological studies of problem gamblers are few, two recent electroencephalography (EEG) studies provide preliminary evidence for neural sensitization in problem gamblers (Hewig et al., 2010; Oberg et al., 2011). "
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    ABSTRACT: The incentive sensitization theory is a promising model for understanding the mechanisms underlying drug addiction, and has received support in animal and human studies. So far the theory has not been applied to the case of behavioral addictions like Gambling Disorder, despite sharing clinical symptoms and underlying neurobiology. We examine the relevance of this theory for Gambling Disorder and point to predictions for future studies. The theory promises a significant contribution to the understanding of behavioral addiction and opens new avenues for treatment.
    Neuroscience & Biobehavioral Reviews 07/2014; 45. DOI:10.1016/j.neubiorev.2014.07.009 · 8.80 Impact Factor
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