Vanja Rozenblat1, Deborah Ong2, Matthew Fuller-Tyszkiewicz3, Kirsti Akkermann4, David Collier5, Rutger C M E Engels6, Fernando Fernandez-Aranda7, Jaanus Harro4, Judith R Homberg8, Andreas Karwautz9, Evelyn Kiive4, Kelly L Klump10, Christine L Larson11, Sarah E Racine10, Jodie Richardson12, Howard Steiger12, Scott F Stoltenberg13, Tatjana van Strien6, Gudrun Wagner9, Janet Treasure14, Isabel Krug2. 1. Department of Psychological Sciences, The University of Melbourne, Parkville 3010, Australia. Electronic address: vanja@rozenblat.net. 2. Department of Psychological Sciences, The University of Melbourne, Parkville 3010, Australia. 3. School of Psychology, Deakin University, Geelong 3220, Australia. 4. Department of Psychology, Estonian Centre of Behavioural and Health Sciences, University of Tartu, Tartu 50410, Estonia. 5. Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College, London SE5 8AF, United Kingdom. 6. Behavioural Science Institute, Radboud University Nijmegen, 6500 HE Nijmegen, The Netherlands. 7. Department of Psychiatry, University Hospital of Bellvitge - IDIBELL, 08907, Spain; CIBER Fisiopatologia Obesidad y Nutricion (CIBERobn), Instituto Salud Carlos III, Madrid, Spain. 8. Donders Institute for Brain, Cognition, and Behaviour, Centre for Neuroscience, Radboud University Medical Centre, Department of Cognitive Neuroscience, 6525 EZ Nijmegen, The Netherlands. 9. Department of Child and Adolescent Psychiatry, Medical University of Vienna, 1090 Vienna, Austria. 10. Department of Psychology, Michigan State University, East Lansing, MI 48824-1116, United States. 11. Department of Psychology, University of Wisconsin-Milwaukee, WI, United States. 12. Eating Disorders Continuum, Douglas Institute, Montreal, Canada; Psychiatry Department, McGill University, Montreal, Canada. 13. Department of Psychology, University of Nebraska-Lincoln, Lincoln, NE 68588, United States. 14. The Institute of Psychiatry, Psychology, and Neuroscience, King's College, London SE5 8AF, United Kingdom.
Abstract
OBJECTIVES: To summarize and synthesize the growing gene x environment (GxE) 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 = 1750, 64.5% female) and two clinical (n = 426, 100% female) samples combined to perform four secondary-data analyses: 5-HTTLPR x Traumatic Life Events to predict ED status (n = 909), 5-HTTLPR x Sexual and Physical Abuse to predict bulimic symptoms (n = 1097), 5-HTTLPR x Depression to predict bulimic symptoms (n = 1256), and 5-HTTLPR x Impulsiveness to predict disordered eating (n = 1149). 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 GxE 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. Copyright Â
OBJECTIVES: To summarize and synthesize the growing gene x environment (GxE) 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 = 1750, 64.5% female) and two clinical (n = 426, 100% female) samples combined to perform four secondary-data analyses: 5-HTTLPRx Traumatic Life Events to predict ED status (n = 909), 5-HTTLPR x Sexual and Physical Abuse to predict bulimic symptoms (n = 1097), 5-HTTLPRx Depression to predict bulimic symptoms (n = 1256), and 5-HTTLPRx Impulsiveness to predict disordered eating (n = 1149). 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 GxE 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. Copyright Â
Authors: Katherine S Button; John P A Ioannidis; Claire Mokrysz; Brian A Nosek; Jonathan Flint; Emma S J Robinson; Marcus R Munafò Journal: Nat Rev Neurosci Date: 2013-04-10 Impact factor: 34.870
Authors: Melanie Achermann; Juliane Günther; Kirstin Goth; Klaus Schmeck; Simone Munsch; Lars Wöckel Journal: Int J Environ Res Public Health Date: 2022-04-04 Impact factor: 3.390