A meta-analysis of gene (5-HTT) × environment interactions in eating pathology using secondary data analyses - 13/04/16

Doi : 10.1016/j.eurpsy.2016.01.035

V. Rozenblat ¹, D. Ng ¹, M. Fuller-Tyszkiewicz ², K. Akkermann ³, D. Collier ⁴, R. Engels ⁵, F. Fernandez-Aranda ⁶, J. Harro ⁷, A. Karwautz ⁸, J. Homberg ⁹, K. Klump ¹⁰, S. Racine ¹¹, C. Larson ¹², H. Steiger ¹³, J. Richardson ¹⁴, S. Stoltenberg ¹⁵, T. van Strien ¹⁶, G. Wagner ⁸, J. Treasure ¹⁷, I. Krug ^18,^⁎
¹ University of Melbourne, Psychological Sciences, Melbourne, Australia
² Deakin University, Psychology, Melbourne, Australia
³ University of Tartu, Psychological, Tartu, Estonia
⁴ King's College London, Social Genetic and Developmental Psychiatry SGDP, London, United Kingdom
⁵ Radboud University, Behavioural Science Institute, Nijmegen, Netherlands
⁶ University of Barcelona, Bellvitge Hospital, Barcelona, Spain
⁷ University of Tartu, Psychology, Tartu, Estonia
⁸ Medical University of Vienna, Psychiatry, Vienna, Austria
⁹ Radbough University, Behavioural Sciences, Nijmegen, Netherlands
¹⁰ Michigan State University, Psychology, Michigan, USA
¹¹ Ohio University, Psychology, Ohio, USA
¹² University of Wisconsin-Milwaukee, Psychology, Wisconsin, USA
¹³ McGill, Psychology, Montreal, Canada
¹⁴ McGill University, Psychiatry, Montreal, Canada
¹⁵ University of Nebraska Lincoln, Psychology, Nebraska, USA
¹⁶ Radboud University, Behavioural Science Institute, Nijmegn, Netherlands
¹⁷ King's College London, Psychological Medicine, London, United Kingdom
¹⁸ University of Melbourne, Psychology, Melbourne, Australia

^⁎Corresponding author.

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Résumé

Background

Gene×environment (G×E) interactions in eating pathology have been increasingly investigated, however studies have been limited by sample size due to the difficulty of obtaining genetic data.

Objective

To synthesize existing G×E research in the eating disorders (ED) field and provide a clear picture of the current state of knowledge with analyses of larger samples.

Method

Complete data from seven studies investigating community (n=1750, 64.5% female) and clinical (n=426, 100% female) populations, identified via systematic review, were included. Data were combined to perform five analyses: 5-HTTLPR×Traumatic Life Events (0–17 events) to predict ED status (n=909), 5-HTTLPR×Sexual and Physical Abuse (n=1097) to predict bulimic symptoms, 5-HTLPR×Depression to predict bulimic symptoms (n=1256), and 5-HTTLPR×Impulsivity to predict disordered eating (n=1149).

Results

The low function (s) allele of 5-HTTLPR interacted with number of traumatic life events (P<.01) and sexual and physical abuse (P<.05) to predict increased likelihood of an ED in females but not males (Fig. 1). No other G×E interactions were significant, possibly due to the medium to low compatibility between datasets (Fig. 1).

Conclusion

Early promising results suggest that increased knowledge of G×E interactions could be achieved if studies increased uniformity of measuring ED and environmental variables, allowing for continued collaboration to overcome the restrictions of obtaining genetic samples.

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