BACKGROUND: Recent studies have raised issues concerning the replicability of gene × environment (G × E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between abuse or maltreatment exposure and antisocial behaviour. This study attempted to replicate the findings in this area using a 30-year longitudinal study that has strong resemblance to the original research cohort. AIMS: To test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to abuse exposure. METHOD: Participants were 398 males from the Christchurch Health and Development Study who had complete data on: MAOA promoter region variable number tandem repeat genotype; antisocial behaviour to age 30; and exposure to childhood sexual and physical abuse. RESULTS: Regression models were fitted to five antisocial behaviour outcomes (self-reported property offending; self-reported violent offending; convictions for property/violent offending; conduct problems; hostility) observed from age 16 to 30, using measures of childhood exposure to sexual and physical abuse. The analyses revealed consistent evidence of G × E interactions, with those having the low-activity MAOA variant and who were exposed to abuse in childhood being significantly more likely to report later offending, conduct problems and hostility. These interactions remained statistically significant after control for a range of potentially confounding factors. Findings for convictions data were somewhat weaker. CONCLUSIONS: The present findings add to the evidence suggesting that there is a stable G × E interaction involving MAOA, abuse exposure and antisocial behaviour across the life course.
BACKGROUND: Recent studies have raised issues concerning the replicability of gene × environment (G × E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between abuse or maltreatment exposure and antisocial behaviour. This study attempted to replicate the findings in this area using a 30-year longitudinal study that has strong resemblance to the original research cohort. AIMS: To test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to abuse exposure. METHOD:Participants were 398 males from the Christchurch Health and Development Study who had complete data on: MAOA promoter region variable number tandem repeat genotype; antisocial behaviour to age 30; and exposure to childhood sexual and physical abuse. RESULTS: Regression models were fitted to five antisocial behaviour outcomes (self-reported property offending; self-reported violent offending; convictions for property/violent offending; conduct problems; hostility) observed from age 16 to 30, using measures of childhood exposure to sexual and physical abuse. The analyses revealed consistent evidence of G × E interactions, with those having the low-activity MAOA variant and who were exposed to abuse in childhood being significantly more likely to report later offending, conduct problems and hostility. These interactions remained statistically significant after control for a range of potentially confounding factors. Findings for convictions data were somewhat weaker. CONCLUSIONS: The present findings add to the evidence suggesting that there is a stable G × E interaction involving MAOA, abuse exposure and antisocial behaviour across the life course.
Authors: Rickard L Sjöberg; Kent W Nilsson; Hanna-Linn Wargelius; Jerzy Leppert; Leif Lindström; Lars Oreland Journal: Am J Med Genet B Neuropsychiatr Genet Date: 2007-03-05 Impact factor: 3.568
Authors: David Huizinga; Brett C Haberstick; Andrew Smolen; Scott Menard; Susan E Young; Robin P Corley; Michael C Stallings; Jennifer Grotpeter; John K Hewitt Journal: Biol Psychiatry Date: 2006-10-01 Impact factor: 13.382
Authors: Nelly Alia-Klein; Rita Z Goldstein; Aarti Kriplani; Jean Logan; Dardo Tomasi; Benjamin Williams; Frank Telang; Elena Shumay; Anat Biegon; Ian W Craig; Fritz Henn; Gene-Jack Wang; Nora D Volkow; Joanna S Fowler Journal: J Neurosci Date: 2008-05-07 Impact factor: 6.167
Authors: Andreas Reif; Michael Rösler; Christine M Freitag; Marc Schneider; Andrea Eujen; Christian Kissling; Denise Wenzler; Christian P Jacob; Petra Retz-Junginger; Johannes Thome; Klaus-Peter Lesch; Wolfgang Retz Journal: Neuropsychopharmacology Date: 2007-03-07 Impact factor: 7.853
Authors: Sean C Godar; Laura J Mosher; Simona Scheggi; Paola Devoto; Kelly M Moench; Hunter J Strathman; Cori M Jones; Roberto Frau; Miriam Melis; Carla Gambarana; Brent Wilkinson; M Graziella DeMontis; Stephen C Fowler; Marcelo P Coba; Cara L Wellman; Jean C Shih; Marco Bortolato Journal: Neuropharmacology Date: 2019-02-01 Impact factor: 5.250
Authors: Mirjam A G Sprangers; Melissa S Y Thong; Meike Bartels; Andrea Barsevick; Juan Ordoñana; Qiuling Shi; Xin Shelley Wang; Pål Klepstad; Eddy A Wierenga; Jasvinder A Singh; Jeff A Sloan Journal: Qual Life Res Date: 2014-03-07 Impact factor: 4.147
Authors: John F Pearson; David M Fergusson; L John Horwood; Allison L Miller; Patrick F Sullivan; Liu E Youfang; Martin A Kennedy Journal: Am J Med Genet B Neuropsychiatr Genet Date: 2012-12-19 Impact factor: 3.568