Attentional bias and response inhibition in severe obesity with food disinhibition: a study of P300 and N200 event-related potential.


Journal

International journal of obesity (2005)
ISSN: 1476-5497
Titre abrégé: Int J Obes (Lond)
Pays: England
ID NLM: 101256108

Informations de publication

Date de publication:
01 2020
Historique:
received: 22 09 2018
accepted: 24 02 2019
revised: 05 02 2019
pubmed: 11 4 2019
medline: 1 12 2020
entrez: 11 4 2019
Statut: ppublish

Résumé

In obesity there is growing evidence for common mechanism between food intake regulation and substance use disorders, especially more attentional bias and less cognitive control. In the present study we investigated whether severely obese subjects with or without disordered eating exhibit electroencephalographic (EEG) event-related potential (ERP) modifications as observed in substance abusers. A total of 90 women were included; 30 in the normal-weight (NW) group (18.5 < BMI < 24.5 kg/m The mean ± SD P300 amplitudes in Pz were significantly (p < 0.05) lower in ObFD- (12.4 ± 4.6) and ObFD+ (12.5 ± 4.4) groups than in the NW group (15.8 ± 5.9). The mean ± SD N200 amplitude in Cz was significantly lower in the ObFD- group (-2.0 ± 5.4) than in the NW group (-5.2 ± 4.2 vs; p = 0.035). N200 Cz amplitude was correlated with EDI-2 Binge eating risk score (ρ = 0.331; p = 0.01), EDI-2 Body Dissatisfaction score (ρ = 0.351; p = 0.007), and Drive for Thinness score (ρ = 0.26; p = 0.05). The present study provides evidence for reduction of P300 and N200 amplitude in obese women and that N200 amplitude may be related to more disordered eating and eating disorder risk. This leads to consider attentional bias and response inhibition as core mechanisms in obesity and as possible targets for new therapeutic strategy.

Sections du résumé

BACKGROUND/OBJECTIVE
In obesity there is growing evidence for common mechanism between food intake regulation and substance use disorders, especially more attentional bias and less cognitive control. In the present study we investigated whether severely obese subjects with or without disordered eating exhibit electroencephalographic (EEG) event-related potential (ERP) modifications as observed in substance abusers.
SUBJECTS/METHODS
A total of 90 women were included; 30 in the normal-weight (NW) group (18.5 < BMI < 24.5 kg/m
RESULTS
The mean ± SD P300 amplitudes in Pz were significantly (p < 0.05) lower in ObFD- (12.4 ± 4.6) and ObFD+ (12.5 ± 4.4) groups than in the NW group (15.8 ± 5.9). The mean ± SD N200 amplitude in Cz was significantly lower in the ObFD- group (-2.0 ± 5.4) than in the NW group (-5.2 ± 4.2 vs; p = 0.035). N200 Cz amplitude was correlated with EDI-2 Binge eating risk score (ρ = 0.331; p = 0.01), EDI-2 Body Dissatisfaction score (ρ = 0.351; p = 0.007), and Drive for Thinness score (ρ = 0.26; p = 0.05).
CONCLUSIONS
The present study provides evidence for reduction of P300 and N200 amplitude in obese women and that N200 amplitude may be related to more disordered eating and eating disorder risk. This leads to consider attentional bias and response inhibition as core mechanisms in obesity and as possible targets for new therapeutic strategy.

Identifiants

pubmed: 30967609
doi: 10.1038/s41366-019-0360-x
pii: 10.1038/s41366-019-0360-x
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

204-212

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Auteurs

Sylvain Iceta (S)

Centre Référent pour l'Anorexie et les Troubles du Comportement Alimentaire (CREATYON), Hospices Civils de Lyon, Lyon, France. sylvain.iceta@chu-lyon.fr.
INSERM U1028, CNRS UMR5292, Université Claude Bernard Lyon 1, Centre de Recherche en Neurosciences de Lyon (CRNL), Equipe PSYR2 Centre Hospitalier Le Vinatier, Lyon, France. sylvain.iceta@chu-lyon.fr.
Centre Intégré de l'Obésité Rhône-Alpes; Fédération Hospitalo-Universitaire DO-iT, Service Endocrinologie-Diabète-Nutrition, Université de Lyon, Groupement Hospitalier Sud, Hospices Civils de Lyon, Lyon, France. sylvain.iceta@chu-lyon.fr.

Julien Benoit (J)

Centre de Recherche en Nutrition Humaine Rhône-Alpes, Univ-Lyon, CarMeN Laboratory, Université Claude Bernard Lyon1, Hospices Civils de Lyon, CENS, FCRIN/FORCE Network, Pierre Benite, France.

Philippe Cristini (P)

Centre de Recherche en Nutrition Humaine Rhône-Alpes, Univ-Lyon, CarMeN Laboratory, Université Claude Bernard Lyon1, Hospices Civils de Lyon, CENS, FCRIN/FORCE Network, Pierre Benite, France.

Stéphanie Lambert-Porcheron (S)

Centre de Recherche en Nutrition Humaine Rhône-Alpes, Univ-Lyon, CarMeN Laboratory, Université Claude Bernard Lyon1, Hospices Civils de Lyon, CENS, FCRIN/FORCE Network, Pierre Benite, France.

Bérénice Segrestin (B)

Centre Référent pour l'Anorexie et les Troubles du Comportement Alimentaire (CREATYON), Hospices Civils de Lyon, Lyon, France.
Centre de Recherche en Nutrition Humaine Rhône-Alpes, Univ-Lyon, CarMeN Laboratory, Université Claude Bernard Lyon1, Hospices Civils de Lyon, CENS, FCRIN/FORCE Network, Pierre Benite, France.

Martine Laville (M)

Centre Intégré de l'Obésité Rhône-Alpes; Fédération Hospitalo-Universitaire DO-iT, Service Endocrinologie-Diabète-Nutrition, Université de Lyon, Groupement Hospitalier Sud, Hospices Civils de Lyon, Lyon, France.
Centre de Recherche en Nutrition Humaine Rhône-Alpes, Univ-Lyon, CarMeN Laboratory, Université Claude Bernard Lyon1, Hospices Civils de Lyon, CENS, FCRIN/FORCE Network, Pierre Benite, France.

Emmanuel Poulet (E)

INSERM U1028, CNRS UMR5292, Université Claude Bernard Lyon 1, Centre de Recherche en Neurosciences de Lyon (CRNL), Equipe PSYR2 Centre Hospitalier Le Vinatier, Lyon, France.

Emmanuel Disse (E)

Centre Intégré de l'Obésité Rhône-Alpes; Fédération Hospitalo-Universitaire DO-iT, Service Endocrinologie-Diabète-Nutrition, Université de Lyon, Groupement Hospitalier Sud, Hospices Civils de Lyon, Lyon, France.
Centre de Recherche en Nutrition Humaine Rhône-Alpes, Univ-Lyon, CarMeN Laboratory, Université Claude Bernard Lyon1, Hospices Civils de Lyon, CENS, FCRIN/FORCE Network, Pierre Benite, France.

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