Association of trait-defined, eating-disorder sub-phenotypes with (biallelic and triallelic) 5HTTLPR variations.
BACKGROUND
Efforts to classify eating-disordered individuals based on concurrent personality traits have consistently converged on a typology encompassing "over-regulated", "dysregulated", and "low psychopathology" subgroups. In various populations, evidence has associated personality variations of an "over-regulated/dysregulated" type with differences on serotonin-system indices, and specifically, with different loadings of serotonin transporter promoter regulatory region polymorphism (5HTTLPR) genotypes and alleles. We explored the extent to which an empirical, trait-defined typology of eating-disordered individuals coincided systematically with variations in 5HTTLPR, assayed using biallelic and triallelic models.


METHODS
We tested 185 women with a DSM-IV eating disorder (108 with Bulimia Nervosa, 17 Anorexia Nervosa, and 60 an Eating Disorder Not Otherwise Specified) and 93 with no eating disorder on measures reflecting psychopathological traits and 5HTTLPR (biallelic and triallelic) genotypes and alleles.


RESULTS
The highest-function, triallelic (L(A)/L(A)) genotype occurred significantly more frequently among eating-disordered individuals than among controls. However, a more fine-grained analysis suggested that this association was attributable to the fact that, among eating-disordered participants, those displaying an "Inhibited/Compulsive" profile (derived using latent class analysis) were more likely than those of a "Dissocial/Impulsive" or a "Low Psychopathology" group to carry the triallelic 5HTTLPR gain-of-function L(A) allele and to be L(A)/L(A) homozygotes.


CONCLUSIONS
This study's empirically derived classes coincide with interpretable differences on genetic indices-associating an "Inhibited/Compulsive" group with 5HTTLPR gain-of-function genotypes (and alleles) that have elsewhere been linked to trait compulsivity. The findings, furthermore, suggest that 5HTTLPR, by influencing personality-trait manifestations may, in turn, influence eating-disorder risk and symptom expression.
Steiger
Howard
H
Eating Disorders Program, Douglas University Institute in Mental Health, Quebec, Canada. stehow@douglas.mcgill.ca
Richardson
Jodie
J
Schmitz
Norbert
N
Joober
Ridha
R
Israel
Mimi
M
Bruce
Kenneth R
KR
Gauvin
Lise
L
Dandurand
Cathy
C
Anestin
Annelie
A
D000293:Adolescent; D000328:Adult; D000856:Anorexia Nervosa; D052018:Bulimia Nervosa; D016009:Chi-Square Distribution; D001068:Feeding and Eating Disorders / Q000145:classification / Q000235:genetics / Q000503:physiopathology; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008875:Middle Aged; D010551:Personality / Q000235:genetics; D010552:Personality Assessment; D010641:Phenotype; D011110:Polymorphism, Genetic / Q000235:genetics*; D011401:Promoter Regions, Genetic / Q000235:genetics*; D011569:Psychiatric Status Rating Scales; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics*; D055815:Young Adult
D050486:Serotonin Plasma Membrane Transport Proteins