Psychoactive substance consumption in eating disorders

Corcos, Maurice; Nezelof, Sylvie; Speranza, Mario; Topa, S.; Girardon, Nicolas; Guilbaud, Olivier; Taïeb, Olivier; Bizouard, P.; Halfon, Olivier; Vénisse, Jean-Luc; Pérez-Díaz, Fernando; Flament, Martine F.; Jeammet, P.

doi:10.1016/s1471-0153(00)00021-0

Cited by 38 publications

(22 citation statements)

References 22 publications

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“…Food ingestion or deprivation, as well as psychoactive substance consumption, would constitute responses to experiencing such intense reactions. The frequency of substance use disorders (alcohol, drugs, psychotropic medications) associated with the increase in eating disorders supports the view that addiction is an important parameter to consider in the process of understanding emotional functioning abilities in eating disorders (Corcos et al, 2001). So does the demonstration of increased secretion of cerebral b-endorphin in patients with anorexia nervosa and bulimia nervosa (Bergh & Soderstein, 1996;Fullerton, 1986;Hawkes, 1992).…”

Section: Discussionmentioning

confidence: 66%

Emotion-processing deficits in eating disorders

Bydlowski

Corcos

Jeammet

et al. 2005

Int. J. Eat. Disord.

287

188

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Section: Discussionmentioning

confidence: 66%

Emotion-processing deficits in eating disorders

Bydlowski

Corcos

Jeammet

et al. 2005

Int. J. Eat. Disord.

287

188

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“…(40). Finally, there is some evidence that eating disorders, particularly bulimia nervosa (BN), are associated with the use of psychoactive substances (41). Most of these human studies point to the pathological basis of food addiction as a real disorder, although the role of dopaminergic neurotransmission in this context is not clear.…”

Section: Food Addictionmentioning

confidence: 99%

Perspective food addiction, caloric restriction, and dopaminergic neurotransmission

Stankowska

Gjedde

2013

Acta Neuropsychiatr.

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Stankowska AUM, Gjedde A. Perspective food addiction, caloric restriction, and dopaminergic neurotransmission.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. Summations> With neurobiological similarities among the brain functions of individuals with behaviour suggestive of addiction, obese individuals with reduced reward sensitivity suffer from pathological addiction to food. > Both undernutrition and dieting are positively correlated with strong craving for food and accompanying overeating, evidently as a compensation for reduced activity of neurobiological reward mechanisms. > The combination of caloric restriction and food addiction alone has a high risk of continued bouts of overeating as results of the reduced gain from dopaminergic neurotransmission maintained by repeated relapses. The risk can be diminished by lifestyle modifications that at the very least include exercise and counselling or group therapy. The inverted U-shaped model is a measure of the efficiency of a given individual's reward system. Considerations> The neurobiological similarities among the brain functions of individuals with behaviour suggestive of addiction suggest but do not prove that obese individuals with reduced reward sensitivity in fact suffer from an addiction.

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“…50% of AN patients will develop bulimic symptoms and migrate to a binge/purge subtype of AN and one third of those with BN have a history of AN (Bulik et al, 1997b;Eckert et al, 1995;Eddy et al, 2007;Eddy et al, 2002;Strober et al, 1997;Tozzi et al, 2005 SMR BN: 2.0 (95% CI) Prevalence Prevalence AN: 0.2 and 0.5% BN: 1.1-4.2% Course and outcome Course and outcome AN: less favourable than BN (Fichter & Quadflieg, 2004) BN: more favourable than AN (Fichter & Quadflieg, 2004) Addiction Liability Addiction Liability AN: AN-R shows significantly less drug-consumption behaviours and alcohol abuse (Corcos et al, 2001) BN: BN shows a significantly higher risk of developing a psychoactive substance dependence during his/her lifetime. (Bulik, 1987;Bulik et al, 1997a;Dansky et al, 2000;Goodman, 2007;Herzog et al, 2006;Holderness et al, 1994;Jones et al, 1985;Lacey, 1993;Mitchell et al, 1985;Mitchell et al, 1991;Welch & Fairburn, 1996;Wilson, 1992) Genetics Genetics Linkage analysis: less number of linkage signals, with minimal overlap with BN (Bacanu et al, 2005) Linkage analysis: greater number of linkage signals, with minimal overlap with AN (Bacanu et al, 2005) Susceptibility locus: chromosome 1 (Grice et al, 2002), 2, and 13 (Devlin et al, 2002) with inclusion of core behavioural covariates Susceptibility locus: chromosome 10p,with a suggestive linkage on chromosome 14 (Bulik et al, 2003 …”

Section: Consistencymentioning

confidence: 99%

“…A person who has been diagnosed with BN is at a significantly higher risk than is the general population to develop, during his or her lifetime, a psychoactive substance dependence (Bulik, 1987;Bulik, Sullivan, Carter, & Joyce, 1997a;Dansky, Brewerton, & Kilpatrick, 2000;Goodman, 2007;Herzog, Franko, Dorer, Keel, Jackson, & Manzo, 2006;Holderness, Brooks-Gunn, & Warren, 1994;Jones, Cheshire, & Moorhouse, 1985;Lacey, 1993;Mitchell et al, 1985;Mitchell, Specker, & de Zwaan, 1991;Welch & Fairburn, 1996;Wilson, 1992). On the other hand, a person who has been diagnosed with AN restrictive (AN-R) shows significantly less drug-consumption behaviours and alcohol abuse and/or dependence disorders than AN binge purge (AN-B) and BN patients (Corcos et al, 2001). This difference in co-morbidity with substance use disorders suggests a different vulnerability to addiction and dependence and possibly the intensity of the addictive behaviours and of the associated co-morbidity (Corcos et al, 2001).…”

Section: Coherencementioning

confidence: 99%