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5-HT2A gene promoter polymorphism as a modifying rather than a vulnerability factor in anorexia nervosa

Published online by Cambridge University Press:  16 April 2020

A. Kipman ,
L. Bruins-Slot ,
C. Boni ,
N. Hanoun ,
J. Adès ,
P. Blot ,
M. Hamon ,
M.-C. Mouren-Siméoni  and
P. Gorwood
A. Kipman
Affiliation:
Hôpital Louis Mourier (AP-HP), Service de Psychiatrie, 178, rue des Renouillers, 92700, Colombes, France Hôpital Robert Debré (AP-HP), Service de Psychopathologie de l'Enfant et de l'Adolescent, Boulevard Serrurier, 75019, Paris, France
L. Bruins-Slot
Affiliation:
Hôpital Louis Mourier (AP-HP), Service de Psychiatrie, 178, rue des Renouillers, 92700, Colombes, France
C. Boni
Affiliation:
INSERM U 288, IFR des Neuroesciences (70), Neuropsychopharmacologie, CHU Pitié-Salpêtrière, 75013, Paris, France
N. Hanoun
Affiliation:
INSERM U 288, IFR des Neuroesciences (70), Neuropsychopharmacologie, CHU Pitié-Salpêtrière, 75013, Paris, France
J. Adès
Affiliation:
Hôpital Louis Mourier (AP-HP), Service de Psychiatrie, 178, rue des Renouillers, 92700, Colombes, France
P. Blot
Affiliation:
Hôpital Robert Debré (AP-HP), Service de Gynécologie-Obstétrique, Boulevard Serrurier, 75019, Paris, France
M. Hamon
Affiliation:
INSERM U 288, IFR des Neuroesciences (70), Neuropsychopharmacologie, CHU Pitié-Salpêtrière, 75013, Paris, France
M.-C. Mouren-Siméoni
Affiliation:
Hôpital Robert Debré (AP-HP), Service de Psychopathologie de l'Enfant et de l'Adolescent, Boulevard Serrurier, 75019, Paris, France CNRS UMR 7593-Paris VII, IFR des Neuroesciences (70), Personnalité et conduites adaptatives, CHU Pitié-Salpêtrière, 75013, Paris, France
P. Gorwood*
Affiliation:
Hôpital Louis Mourier (AP-HP), Service de Psychiatrie, 178, rue des Renouillers, 92700, Colombes, France CNRS UMR 7593-Paris VII, IFR des Neuroesciences (70), Personnalité et conduites adaptatives, CHU Pitié-Salpêtrière, 75013, Paris, France
*
Corresponding author. E-mail address: [email protected] (P. Gorwood).
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Summary

The A allele of the 5-HT2A gene (–1438A/G polymorphism) has been associated with anorexia nervosa in four studies, but not in three others. One possibility to explain such a discrepancy is that the A allele acts as a modifying rather than a vulnerability allele. To test this hypothesis, we increased our initial sample of 102 trios [Mol. Psychiatry 7 (2002) 90] with 43 new patients with anorexia nervosa and 98 healthy controls. In addition to confirming the absence of association on the global sample of 145 patients, we found that patients with the A allele had a significantly later age at onset of the disease (P = 0.032). Furthermore, the A allele was also transmitted with an older age at onset (P = 0.023) using a quantitative-trait TDT approach. The A allele may thus act as a modifying factor (delaying onset), potentially explaining variations of allele frequency across samples, in which differences in average age at onset are not only possible, but also expected. Taking into account vulnerability genes, but also genes modifying the expression of the disorder, will help to disentangle the complexity of the etiological factors involved in anorexia nervosa.

Keywords

Eating disorderAge at onsetSerotoninQuantitative traits
Type
Short Communications
Information
European Psychiatry , Volume 17 , Issue 4 , July 2002 , pp. 227 - 229
Copyright
Copyright © Éditions scientifiques et médicales Elsevier SAS 2002

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