Perspective food addiction, caloric restriction, and dopaminergic neurotransmission

Arwen Urrsula Malgorzata Stankowska, Albert Gjedde

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)257-267
Number of pages11
JournalActa Neuropsychiatrica
Volume25
Issue number5
DOIs
StatePublished - Oct 2013

Fingerprint

Caloric Restriction
Synaptic Transmission
Habits
Food
Dopamine Receptors
Reward
Dopamine
Eating
Recurrence
Bulimia
Neurobiology
Nucleus Accumbens
Street Drugs
Feeding Behavior
Drug Users
Basal Ganglia
Malnutrition
Cerebral Cortex
Life Style
Obesity

Keywords

  • dopamine
  • Keywords caloric restriction
  • reinforcement
  • reward
  • substance-related disorders

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Biological Psychiatry

Cite this

Perspective food addiction, caloric restriction, and dopaminergic neurotransmission. / Stankowska, Arwen Urrsula Malgorzata; Gjedde, Albert.

In: Acta Neuropsychiatrica, Vol. 25, No. 5, 10.2013, p. 257-267.

Research output: Contribution to journalArticle

Stankowska, Arwen Urrsula Malgorzata ; Gjedde, Albert. / Perspective food addiction, caloric restriction, and dopaminergic neurotransmission. In: Acta Neuropsychiatrica. 2013 ; Vol. 25, No. 5. pp. 257-267.
@article{2df5f708f87b42e1ac4a344390c99576,
title = "Perspective food addiction, caloric restriction, and dopaminergic neurotransmission",
abstract = "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.",
keywords = "dopamine, Keywords caloric restriction, reinforcement, reward, substance-related disorders",
author = "Stankowska, {Arwen Urrsula Malgorzata} and Albert Gjedde",
year = "2013",
month = "10",
doi = "10.1017/neu.2013.18",
language = "English (US)",
volume = "25",
pages = "257--267",
journal = "Acta Neuropsychiatrica",
issn = "0924-2708",
publisher = "Wiley-Blackwell",
number = "5",

}

TY - JOUR

T1 - Perspective food addiction, caloric restriction, and dopaminergic neurotransmission

AU - Stankowska, Arwen Urrsula Malgorzata

AU - Gjedde, Albert

PY - 2013/10

Y1 - 2013/10

N2 - 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.

AB - 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.

KW - dopamine

KW - Keywords caloric restriction

KW - reinforcement

KW - reward

KW - substance-related disorders

UR - http://www.scopus.com/inward/record.url?scp=84884771449&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84884771449&partnerID=8YFLogxK

U2 - 10.1017/neu.2013.18

DO - 10.1017/neu.2013.18

M3 - Article

AN - SCOPUS:84884771449

VL - 25

SP - 257

EP - 267

JO - Acta Neuropsychiatrica

JF - Acta Neuropsychiatrica

SN - 0924-2708

IS - 5

ER -