Dopamine and Opioid Neurotransmission in Behavioral Addictions: A Comparative PET Study in Pathological Gambling and Binge Eating.
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ABSTRACT:
SUBMITTER: Majuri J
PROVIDER: S-EPMC5357051 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Central dopaminergic mechanisms are involved in the motivational aspects of eating and food choices. This review focuses on human and animal data investigating the importance of dopamine on binge eating behaviors. Early work examining dopamine metabolites in the cerebrospinal fluid and plasma of bulimic individuals suggested decreased dopamine turnover during the active phase of the illness. While neuroimaging studies of dopamine mechanisms in bulimia nervosa (BN) and binge eating disorder (BED) are limited, genetic studies in humans have implicated an increased frequency of dopamine transporter and associated D2 receptor polymorphisms with binge pathology. Recent studies in rodent models of dietary-induced binge eating (DIBE) have investigated plausible dopamine mechanisms involved in sustaining binge eating behaviors. In DIBE models, highly palatable foods (fats, sugars and their combination), as well as restricted access conditions appear to promote ingestive responses and result in sustained dopamine stimulation within the nucleus accumbens. Taken together with studies on the comorbidity of illicit drug use and eating disorders, the data reviewed here support a role for dopamine in perpetuating the compulsive feeding patterns of BN and BED. As such, we propose that sustained stimulation of the dopamine systems by bingeing promoted by preexisting conditions (e.g., genetic traits, dietary restraint, stress, etc.) results in progressive impairments of dopamine signaling. To disrupt this vicious cycle, novel research-based treatment options aiming at the neural substrates of compulsive eating patterns are necessary.
| S-EPMC2977997 | biostudies-literature
Project description:BACKGROUND:Binge eating is associated with obesity and has been conceptualized as "food addiction." However, this view has received only inconsistent support in humans, and limited evidence relates key neurocircuitry to the disorder. Moreover, relatively few studies have used pharmacologic functional magnetic resonance imaging to probe the underlying basis of altered eating behaviors. METHODS:In a double-blind, placebo-controlled, parallel group study, we explored the effects of a potent mu-opioid receptor antagonist, GSK1521498, in obese individuals with moderate binge eating. Subjects were tested during a baseline placebo run-in period and retested after 28-days of drug (n = 21) or placebo (n = 21) treatment. Using functional magnetic resonance imaging and behavioral measures, we determined the drug's effects on brain responses to food images and, separately, on motivation to expend energy to view comparable images. RESULTS:Compared with placebo, GSK1521498 was associated with a significant reduction in pallidum/putamen responses to pictures of high-calorie food and a reduction in motivation to view images of high-calorie food. Intriguingly, although motivational responding was reduced, subjective liking for the same images actually increased following drug treatment. CONCLUSIONS:Stimulus-specific putamen/pallidal responses in obese people with binge eating are sensitive to altered mu-opioid function. This neuromodulation was accompanied by reductions in motivational responding, as measured by grip force, although subjective liking responses to the same stimuli actually increased. As well as providing evidence for a link between the opioid system and food-related behavior in binge-eating obese individuals, these results support a dissociation across measures of motivation and liking associated with food-related stimuli in these individuals.
| S-EPMC3898083 | biostudies-literature
Project description:ObjectiveBinge eating, a core diagnostic symptom in binge eating disorder and bulimia nervosa, increases the risk of multiple physiological and psychiatric disorders. The neurotransmitter dopamine is involved in food craving, decision making, executive functioning, and impulsivity personality trait; all of which contribute to the development and maintenance of binge eating. The objective of this paper is to review the associations of dopamine levels/activities, dopamine regulator (e.g., dopamine transporter, degrading enzymes) levels/activities, and dopamine receptor availability/affinity with binge eating.MethodsA literature search was conducted in PubMed and PsycINFO to obtain human and animal studies published since 2010.ResultsA total of 31 studies (25 human, six animal) were included. Among the human studies, there were 12 case-control studies, eight randomized controlled trials, and five cross-sectional studies. Studies used neuroimaging (e.g., positron emission tomography), genetic, and pharmacological (e.g., dopamine transporter inhibitor) techniques to describe or compare dopamine levels/activities, dopamine transporter levels/activities, dopamine degrading enzyme (e.g., catechol-O-methyltransferase) levels/activities, and dopamine receptor (e.g., D1, D2) availability/affinity among participants with and without binge eating. Most human and animal studies supported an altered dopaminergic state in binge eating (26/31, 83.9%); however, results were divergent regarding whether the altered state was hyperdopaminergic (9/26, 34.6%) or hypodopaminergic (17/26, 65.4%). The mixed findings may be partially explained by the variability in sample characteristics, study design, diagnosis criteria, and neuroimaging/genetic/pharmacological techniques used. However, it is possible that instead of being mutually exclusive, the hyperdopaminergic and hypodopaminergic state may co-exist, but in different stages of binge eating or in different individual genotypes.ConclusionsFor future studies to clarify the inconsistent findings, a homogenous sample that controls for confounders that may influence dopamine levels (e.g., psychiatric diseases) is preferable. Longitudinal studies are needed to evaluate whether the hyper- and hypo-dopaminergic states co-exist in different stages of binge eating or co-exist in individual phenotypes. Binge eating is characterized by eating a large amount of food in a short time and a feeling of difficulty to stop while eating. Binge eating is the defining symptom of binge eating disorder and bulimia nervosa, both of which are associated with serious health consequences. Studies have identified several psychological risk factors of binge eating, including a strong desire for food, impaired cognitive skills, and distinct personality traits (e.g., quick action without careful thinking). However, the physiological markers of binge eating remain unclear. Dopamine is a neurotransmitter that is heavily involved in feeding behavior, human motivation, cognitive ability, and personality. Therefore, dopamine is believed to play a critical role in binge eating. This review synthesized study findings related to the levels and activities of dopamine, dopamine regulators, and dopamine receptors in the context of binge eating. The primary finding is that most studies that used neuroimaging, genetic, or drug techniques found an altered dopaminergic state related to binge eating. However, the literature is inconsistent concerning the direction of the alteration. Considering the mixed findings and the limitations in study design, future studies, especially those that include repeated measurements, are needed to clarify the role of dopamine in binge eating.
| S-EPMC8796589 | biostudies-literature
Project description:Pathological gambling (PG), a disorder currently categorized as an impulse-control disorder but being considered as a nonsubstance addiction in Diagnostic and Statistical Manual of Mental Disorders (5th ed.) discussions, represents a significant public health concern. Over the past decade, considerable advances have been made with respect to understanding the biological underpinnings of PG. Research has also demonstrated the efficacies of multiple treatments, particularly behavioral therapies, for treating PG. Despite these advances, relatively little is known regarding how biological measures, particularly those assessing brain function, relate to treatments for PG. In this article, we present a conceptual review focusing on the neurobiology of behavioral therapies for PG. To illustrate issues related to study design, we present proof-of-concept preliminary data that link Stroop-related brain activations prior to treatment onset to treatment outcome in individuals with PG receiving a cognitive-behavioral treatment incorporating aspects of imaginal desensitization and motivational interviewing. We conclude with recommendations about current and future directions regarding how to incorporate and translate biological findings into improved therapies for individuals with nonsubstance and substance addictions.
| S-EPMC3700568 | biostudies-literature
Project description:Binge eating disorder is an addiction-like disorder characterized by excessive food consumption within discrete periods of time. This study was aimed at understanding the role of the opioid system within the medial prefrontal cortex (mPFC) in the consummatory and motivational aspects of binge-like eating. For this purpose, we trained male rats to obtain either a sugary, highly palatable diet (Palatable rats) or a chow diet (Chow rats) for 1 hour/day. We then evaluated the effects of the opioid receptor antagonist, naltrexone, given either systemically or site-specifically into the nucleus accumbens (NAcc) or the mPFC on a fixed ratio 1 (FR1) and a progressive ratio schedule of reinforcement for food. Finally, we assessed the expression of the genes proopiomelanocortin (POMC), pro-dynorphin (PDyn) and pro-enkephalin (PEnk), coding for the opioids peptides in the NAcc and the mPFC in both groups. Palatable rats rapidly escalated their intake by four times. Naltrexone, when administered systemically and into the NAcc, reduced FR1 responding for food and motivation to eat under a progressive ratio in both Chow and Palatable rats; conversely, when administered into the mPFC, the effects were highly selective for binge eating rats. Furthermore, we found a twofold increase in POMC and a ?50% reduction in PDyn gene expression in the mPFC of Palatable rats, when compared to control rats; however, no changes were observed in the NAcc. Our data suggest that neuroadaptations of the opioid system in the mPFC occur following intermittent access to highly palatable food, which may be responsible for the development of binge-like eating.
| S-EPMC3664255 | biostudies-literature
Project description:To review the transparency of reports of behavioral interventions for pathological gambling and other gambling-related disorders.We used the Transparent Reporting of Evaluations with Nonrandomized Designs (TREND) Statement to develop the 59-question adapted TREND questionnaire (ATQ). Each ATQ question corresponds to a transparency guideline and asks how clearly a study reports its objectives, research design, analytical methods and conclusions. A subset of 23 ATQ questions is considered particularly important. We searched PubMed, PsychINFO and Web of Science to identify experimental evaluations published between 2000 and 2011 aiming to reduce problem gambling behaviors or decrease problems caused by gambling. Twenty-six English-language reports met the inclusion criteria and were reviewed by three abstractors using the ATQ.The average report adhered to 38.4 (65.1%) of the 59 ATQ transparency guidelines. Each of the 59 ATQ questions received positive responses from an average of 16.9 (63.8%) of the reports. The subset of 23 particularly relevant questions received an average of 15.3 (66.5%) positive responses. Thirty-two of 59 (54%) ATQ questions were answered positively by 75% or more of the study reports, while 12 (20.3%) received positive responses by 25% or fewer. Publication year did not affect these findings.Gambling intervention reports need to improve their transparency by adhering to currently neglected and particularly relevant guidelines. Among them are recommendations for comparing study participants who are lost to follow-up and those who are retained, comparing study participants with the target population, describing methods used to minimize potential bias due to group assignment, and reporting adverse events or unintended effects.
| S-EPMC3401241 | biostudies-literature
Project description:Endogenous opioids, and in particular ?-opioid receptors, have been linked to hedonic and rewarding mechanisms engaged during palatable food intake. The aim of this study was to investigate the effects of GSK1521498, a novel ?-opioid receptor antagonist, on food-seeking behavior and on binge-like eating of a highly preferred chocolate diet. Food seeking was measured in rats trained to respond for chocolate under a second-order schedule of reinforcement, in which prolonged periods of food-seeking behavior were maintained by contingent presentation of a reward-associated conditioned reinforcer. After reaching a stable baseline in both procedures, animals were treated with GSK1521498 (0.1, 1, and 3?mg/kg; IP) or naltrexone (NTX, 0.1, 1, and 3?mg/kg; SC). The binge eating model was characterized by four temporally contiguous phases: 1-h chow access, 2-h food deprivation, 10-min chow access, and 10-min access to either chocolate-flavoured food or standard chow. During training the rats developed binge-like hyperphagia of palatable food and anticipatory chow hypophagia (anticipatory negative contrast). Both compounds reduced binge-like palatable food hyperphagia. However, GSK1521498 reduced the impact of high hedonic value on ingestion more specifically than NTX, abolishing anticipatory chow hypophagia. GSK1521498 also dose-dependently reduced food seeking both before and after food ingestion, whereas NTX reduced food seeking only after food ingestion. Thus, while both drugs affected the hedonic value of the preferred food, GSK1521498 also directly decreased incentive motivation for chocolate. Selective ?-opioid receptor antagonism by GSK1521498 may have utility as a treatment for reducing maladaptive, palatability-driven eating behavior by reducing the motivational properties of stimuli that elicit the binge eating commonly associated with obesity.
| S-EPMC3473330 | biostudies-literature
Project description:ObjectiveDespite proven efficacy of cognitive behavioral therapy (CBT) for treating eating disorders with binge eating as the core symptom, few patients receive CBT in clinical practice. Our blended efficacy-effectiveness study sought to evaluate whether a manual-based guided self-help form of CBT (CBT-GSH), delivered in 8 sessions in a health maintenance organization setting over a 12-week period by master's-level interventionists, is more effective than treatment as usual (TAU).MethodIn all, 123 individuals (mean age = 37.2; 91.9% female, 96.7% non-Hispanic White) were randomized, including 10.6% with bulimia nervosa (BN), 48% with binge eating disorder (BED), and 41.4% with recurrent binge eating in the absence of BN or BED. Baseline, posttreatment, and 6- and 12-month follow-up data were used in intent-to-treat analyses.ResultsAt 12-month follow-up, CBT-GSH resulted in greater abstinence from binge eating (64.2%) than TAU (44.6%; number needed to treat = 5), as measured by the Eating Disorder Examination (EDE). Secondary outcomes reflected greater improvements in the CBT-GSH group in dietary restraint (d = 0.30); eating, shape, and weight concern (ds = 0.54, 1.01, 0.49, respectively; measured by the EDE Questionnaire); depression (d = 0.56; Beck Depression Inventory); and social adjustment (d = 0.58; Work and Social Adjustment Scale), but not weight change.ConclusionsCBT-GSH is a viable first-line treatment option for the majority of patients with recurrent binge eating who do not meet diagnostic criteria for BN or anorexia nervosa.
| S-EPMC2880824 | biostudies-literature
Project description:ObjectiveConsistent self-monitoring of dietary intake, weight, and physical activity predicts better outcomes during behavioral weight loss, but the factors that influence self-monitoring adherence are not well understood. This study attempted to fill gaps in the existing literature by examining whether pre-treatment eating behaviors predict adherence to digital self-monitoring during a behavioral weight loss program.MethodParticipants (N = 77) reported on binge eating, uncontrolled eating, and emotional eating at baseline, and were instructed to self-monitor their food intake, weight, and physical activity using digital devices (food logging app, Fitbit, and wireless "smart" scale) throughout the 12-week treatment. Adherence to self-monitoring was assessed using data captured from these devices.ResultsGreater baseline binge eating severity predicted greater adherence to self-monitoring of weight (ρ = 0.25, p = .03) and eating (ρ = 0.25, p = .03), but not self-monitoring of physical activity. Uncontrolled eating and emotional eating did not significantly predict self-monitoring adherence.ConclusionsIn contrast to previous research, this study found that participants with greater pre-treatment binge eating severity had better adherence to self-monitoring of eating, and for the first time established a relationship between binge eating severity and digital self-monitoring of weight in behavioral weight loss. Individuals with greater pre-treatment binge eating may exhibit characteristics, such as motivation or rigidity, that are beneficial during the initial period of weight loss. Future studies should determine if there are features of analogue versus digital self-monitoring that may explain this pattern of findings, and examine these associations longitudinally.
| S-EPMC7704883 | biostudies-literature
Project description:BackgroundPremature responding is a form of motor impulsivity that preclinical evidence has shown to predict compulsive drug seeking but has not yet been studied in humans. We developed a novel translation of the task, based on the rodent 5-choice serial reaction time task, testing premature responding in disorders of drug and natural food rewards.MethodsAbstinent alcohol- (n = 30) and methamphetamine-dependent (n = 23) subjects, recreational cannabis users (n = 30), and obese subjects with (n = 30) and without (n = 30) binge eating disorder (BED) were compared with matched healthy volunteers and tested on the premature responding task.ResultsCompared with healthy volunteers, alcohol- and methamphetamine-dependent subjects and cannabis users showed greater premature responding with no differences observed in obese subjects with or without BED. Current smokers exhibited greater premature responding versus ex-smokers and nonsmokers. Alcohol-dependent subjects also had lower motivation for explicit monetary incentives. A Motivation Index correlated negatively with alcohol use and binge eating severity.ConclusionsPremature responding on a novel translation of a serial reaction time task was more evident in substance use disorders but not in obese subjects with or without BED. Lower motivation for monetary incentives linked alcohol use and binge eating severity. Our findings add to understanding the relationship between drug and natural food rewards.
| S-EPMC3988873 | biostudies-literature