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Perspective food addiction, caloric restriction, and dopaminergic neurotransmission

Published online by Cambridge University Press:  28 May 2013

Arwen Urrsula Malgorzata Stankowska*
Department of Human Nutrition, University of Copenhagen, Copenhagen, Denmark
Albert Gjedde
Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark Center for Healthy Aging, Faculty of Health Sciences, University of Copenhagen, Blegdamsvej, Copenhagen, Denmark Center of Functionally Integrative Neuroscience, Aarhus University, Aarhus, Denmark McConnell Brain Imaging Center, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada Department of Radiology and Radiological Science, Johns Hopkins University, Baltimore, Maryland, USA
Arwen U. M. Stankowska, Department of Human Nutrition, University of Copenhagen, Rolighedsvej 30, 1958 Frederiksberg C, Copenhagen, Denmark. Tel: +45 53347600; Fax: +45 3536 0116; E-mail:


People attempt to change their lifestyle when obesity impairs their quality of life. The attempts often fail when multiple habits must be changed in unison. Here we explore relations among food addiction, the neurobiology of habits, and caloric restriction, when people seek to return to normal eating behaviour, with particular emphasis on the role of dopaminergic neurotransmission.

Severely obese individuals have specific neurobiological characteristics in common with drug abusers, including low availability of dopamine receptors in the striatum, impaired neuronal responses to dopamine, and reduced activity in prefrontal regions of the cerebral cortex. The neurobiological characteristics suggest that obese people also have a pathological dependence in common with addicts, in the form of food addiction.

Malnutrition and dieting both relate to binge eating, possibly as a compensation for a reduced cognitive reward condition. The combination of caloric restriction and food addiction imparts a high risk of relapse as a result of further reduction of dopaminergic neurotransmission and the subsequent loss of reward. As with drugs of abuse, ingestion of large quantities of sugar in circumstances of uncontrolled eating increases dopamine release in the nucleus accumbens. This and other evidence suggests that abuse of food is a habit learned by means of mechanisms centred in the basal ganglia, with an increased risk of relapse in the presence of associative amplifiers. This risk is predicted by the relationship between dopamine receptor availability in the striatum and sensation-seeking in the form of an inverted U, suggested by recent findings, consistent with two opposite states of hypodopaminergic and hyperdopaminergic neuromodulation.

Review Article
Copyright © Scandinavian College of Neuropsychopharmacology 2013 

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