Genes involved in 5HT transmission have been supposed to contribute to the biologic vulnerability for bulimia nervosa (BN). Because a long (L) and a short (S) variant of the promoter region of the 5HT transporter gene have been identified, we tested whether the 5HTT gene-linked polymorphic region (5HTTLPR) could represent a susceptibility factor for BN and/or could be related to nutritional parameters, harm avoidance personality dimension, and psychiatric comorbidity.
A total of 219 white women (125 bulimics and 94 healthy control subjects) underwent a blood sample collection for 5HTTLPR genotyping and a clinical evaluation assessing comorbidity for axis I and II psychiatric disorders, harm avoidance personality dimension, and body composition (only patients).
The distribution of the 5HTTLPR genotypes did not significantly differ between patients and control subjects, although the L allele was significantly more frequent in the former. Bulimic individuals carrying at least one copy of the S allele had significantly lower mean body mass index and body fat mass values and significantly higher mean harm avoidance score than patients with the LL genotype. No significant association was found between the 5HTTLPR genotype and comorbid axis I and II psychiatric disorders.
These findings support the view that polymorphic variants of the 5HTT promoter region do not play a part in predisposing to BN, whereas they seem to predispose bulimic individuals to nutritional impairment and increased harm avoidance.
ANOVA = analysis of variance; BMI = body mass index; BW = body weight; BN = bulimia nervosa; MINI = Mini International Neuropsychiatric Interview; NS = not significant; 5HT = serotonin; 5HTT = serotonin transporter; 5HTTLPR = serotonin transporter length polymorphic region; SCID-IP = Structured Clinical Interview for DSM IV Axis I disorders–Patient Edition; SCID-II = Structured Clinical Interview for DSM IV Axis II personality disorders; TCI-R = Temperament and Character Inventory Revised.
From the Department of Psychiatry (P.M., A.F., E.C., M.M.), University of Naples SUN, Naples, Italy; the Department of Neurology and Psychiatry (P.S., A.F.), University of Padua, Padua, Italy; the Department of Psychiatry, Neurobiology, Pharmacology and Biotechnologies (M.M., A.R.), University of Pisa, Pisa, Italy; and the Istituto Scientifico Ospedale San Raffaele (L.B., S.E.), Vita-Salute University, Faculty of Psychology, Milan, Italy.
Address correspondence and reprint requests to Palmiero Monteleone, MD, Department of Psychiatry, University of Naples S.U.N., Largo Madonna delle Grazie, 80138 Naples, Italy. E-mail: email@example.com
Received for publication March 31, 2005; revision received August 3, 2005.
Supported by grant n. MM06493915_001 of the Italian Ministry of University and Scientific Research.