The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
Dopamine and binge eating behaviors
Open accessAbstract
Central dopaminergic mechanisms are involved in the motivational aspects of eating and food choices. This review focuses on human and animal data examining the importance of dopamine on binge eating behaviors. Early works 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 examinations of 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 examining 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.
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Cites
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“Aside from the study by Bowers and colleagues, evidence to date suggests that peripheral and central HVA levels are lower during BN. Reduced HVA levels are typically considered an index of reduced dopamine function and reduced dopamine turnover (dopamine to HVA ratio).”
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Cited by
The neurobiological basis of binge-eating disorder
Kessler, R. M., Hutson, P. H., Herman, B. K., & Potenza, M. N. (2016) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2016.01.013 · Cited by 357
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
Feeding and reward: Perspectives from three rat models of binge eating
Corwin, R. L., Avena, N. M., & Boggiano, M. M. (2011) · Physiology & Behavior · doi:10.1016/j.physbeh.2011.04.041 · Cited by 289
The link between stress and feeding behaviour
Maniam, J., & Morris, M. J. (2012) · Neuropharmacology · doi:10.1016/j.neuropharm.2012.04.017 · Cited by 255
Parasomnias: An Updated Review
Howell, M. J. (2012) · Neurotherapeutics · doi:10.1007/s13311-012-0143-8 · Cited by 165
Metadata
- Authors
- Bello, N. T., & Hajnal, A.
- Venue
- Pharmacology Biochemistry and Behavior
- Publisher
- Elsevier BV
- Published
- 2010-11
- Volume
- 97
- Issue
- 1
- Pages
- 25-33
- ISSN
- 0091-3057 (ISSN-L)
- OpenAlex
- W1989014835
- Cited by
- 175
- References
- 22
- FWCI
- 10.84
- Type
- journal article
- Language
- en
- Open access
- green
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