A Systematic Review and Secondary Data Analysis of the Interactions between the Serotonin Transporter 5-HTTLPR Polymorphism and Environmental and Psychological Factors in Eating Disorders

Authors

Vanja Rozenblat, University of MelbourneFollow
Deborah Ong, University of Melbourne
Matthew Fuller-Tyszkiewicz, Deakin UniversityFollow
Kirsti Akkermann, University of TartuFollow
David Collier, King's College
Rutger C. M. E. Engels, Radboud University Nijmegen
Fernando Fernandez-Aranda, University Hospital of Bellvitge-IDIBELL
Jaanus Harro, University of TartuFollow
Judith R. Homberg, Radboud University NijmegenFollow
Andreas Karwautz, Medical University of ViennaFollow
Evelyn Kiive, University of TartuFollow
Kelly K. Klump, Michigan State University
Sarah E. Racine, Michigan State University
Jodie Richardson, Douglas Institute and McGill University
Howard Steiger, Douglas Institute and McGill UniversityFollow
Scott F. Stoltenberg, University of Nebraska-LincolnFollow
Tatjana van Strien, Radboud University NijmegenFollow
Gudrun Wagner, Medical University of Vienna
Janet Treasure, King's CollegeFollow
Isabel Krug, University of Melbourne

Document Type

Article

Date of this Version

1-2017

Citation

Journal of Psychiatric Research 84 (January 2017), pp. 62–72.

doi: 10.1016/j.jpsychires.2016.09.023

Comments

Copyright © 2016 Elsevier Ltd. Used by permission.

Abstract

Objectives: To summarize and synthesize the growing gene × environment (G × E) research investigating the promoter region of the serotonin transporter gene (5-HTTLPR) in the eating disorders (ED) field, and overcome the common limitation of low sample size, by undertaking a systematic review followed by a secondary data meta-analysis of studies identified by the review. Method: A systematic review of articles using PsycINFO, PubMed, and EMBASE was undertaken to identify studies investigating the interaction between 5-HTTLPR and an environmental or psychological factor, with an ED-related outcome variable. Seven studies were identified by the systematic review, with complete data sets of five community (n = 1,750, 64.5% female) and two clinical (n = 426, 100% female) samples combined to perform four secondary-data analyses: 5-HTTLPR × Traumatic Life Events to predict ED status (n = 909), 5-HTTLPR × Sexual and Physical Abuse to predict bulimic symptoms (n = 1,097), 5-HTTLPR × Depression to predict bulimic symptoms (n = 1,256), and 5-HTTLPR × Impulsiveness to predict disordered eating (n = 1,149). Results: Under a multiplicative model, the low function (s) allele of 5-HTTLPR interacted with traumatic life events and experiencing both sexual and physical abuse (but not only one) to predict increased likelihood of an ED and bulimic symptoms, respectively. However, under an additive model there was also an interaction between sexual and physical abuse considered independently and 5-HTTLPR, and no interaction with traumatic life events. No other G × E interactions were significant. Conclusion: Early promising results should be followed-up with continued cross-institutional collaboration in order to achieve the large sample sizes necessary for genetic research.