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Alcoholism: Clinical and Experimental Research

Volume 33, Issue 3

Effects of MAOA‐Genotype, Alcohol Consumption, and Aging on Violent Behavior

Roope Tikkanen

From the Institute of Clinical Medicine, Department of Psychiatry (RT, MH, MV), University of Helsinki, Helsinki, Finland; NIH/NIAAA, Laboratory of Neurogenetics (RLS, DG), Rockville, Maryland; Center for Clinical Research, Uppsala University (RLS), Västerås, Sweden; Department of Neurosurgery (RLS), University Hospital, Umeå, Sweden; King’s College (FD), London, UK; and Department of Forensic Psychiatry and Clinical Physiology (JT), University of Kuopio, Niuvanniemi Hospital, Kuopio, Finland.

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Rickard L. Sjöberg

From the Institute of Clinical Medicine, Department of Psychiatry (RT, MH, MV), University of Helsinki, Helsinki, Finland; NIH/NIAAA, Laboratory of Neurogenetics (RLS, DG), Rockville, Maryland; Center for Clinical Research, Uppsala University (RLS), Västerås, Sweden; Department of Neurosurgery (RLS), University Hospital, Umeå, Sweden; King’s College (FD), London, UK; and Department of Forensic Psychiatry and Clinical Physiology (JT), University of Kuopio, Niuvanniemi Hospital, Kuopio, Finland.

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Francesca Ducci

From the Institute of Clinical Medicine, Department of Psychiatry (RT, MH, MV), University of Helsinki, Helsinki, Finland; NIH/NIAAA, Laboratory of Neurogenetics (RLS, DG), Rockville, Maryland; Center for Clinical Research, Uppsala University (RLS), Västerås, Sweden; Department of Neurosurgery (RLS), University Hospital, Umeå, Sweden; King’s College (FD), London, UK; and Department of Forensic Psychiatry and Clinical Physiology (JT), University of Kuopio, Niuvanniemi Hospital, Kuopio, Finland.

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David Goldman

From the Institute of Clinical Medicine, Department of Psychiatry (RT, MH, MV), University of Helsinki, Helsinki, Finland; NIH/NIAAA, Laboratory of Neurogenetics (RLS, DG), Rockville, Maryland; Center for Clinical Research, Uppsala University (RLS), Västerås, Sweden; Department of Neurosurgery (RLS), University Hospital, Umeå, Sweden; King’s College (FD), London, UK; and Department of Forensic Psychiatry and Clinical Physiology (JT), University of Kuopio, Niuvanniemi Hospital, Kuopio, Finland.

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Matti Holi

From the Institute of Clinical Medicine, Department of Psychiatry (RT, MH, MV), University of Helsinki, Helsinki, Finland; NIH/NIAAA, Laboratory of Neurogenetics (RLS, DG), Rockville, Maryland; Center for Clinical Research, Uppsala University (RLS), Västerås, Sweden; Department of Neurosurgery (RLS), University Hospital, Umeå, Sweden; King’s College (FD), London, UK; and Department of Forensic Psychiatry and Clinical Physiology (JT), University of Kuopio, Niuvanniemi Hospital, Kuopio, Finland.

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Jari Tiihonen

From the Institute of Clinical Medicine, Department of Psychiatry (RT, MH, MV), University of Helsinki, Helsinki, Finland; NIH/NIAAA, Laboratory of Neurogenetics (RLS, DG), Rockville, Maryland; Center for Clinical Research, Uppsala University (RLS), Västerås, Sweden; Department of Neurosurgery (RLS), University Hospital, Umeå, Sweden; King’s College (FD), London, UK; and Department of Forensic Psychiatry and Clinical Physiology (JT), University of Kuopio, Niuvanniemi Hospital, Kuopio, Finland.

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Matti Virkkunen

From the Institute of Clinical Medicine, Department of Psychiatry (RT, MH, MV), University of Helsinki, Helsinki, Finland; NIH/NIAAA, Laboratory of Neurogenetics (RLS, DG), Rockville, Maryland; Center for Clinical Research, Uppsala University (RLS), Västerås, Sweden; Department of Neurosurgery (RLS), University Hospital, Umeå, Sweden; King’s College (FD), London, UK; and Department of Forensic Psychiatry and Clinical Physiology (JT), University of Kuopio, Niuvanniemi Hospital, Kuopio, Finland.

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First published: 19 February 2009
https://doi.org/10.1111/j.1530-0277.2008.00853.x
Cited by: 32
Reprint requests: Roope Tikkanen, MD, Department of Psychiatry, University of Helsinki, PO Box 590, 00029 HUS, Finland; Fax: +358‐9‐471‐63759; E‐mail: roope.tikkanen@helsinki.fi

Abstract

Background: Environmental factors appear to interact with a functional polymorphism (MAOA‐LPR) in the promoter region of the monoamine oxidase A gene (MAOA) in determining some forms of antisocial behavior. However, how MAOA‐LPR modulates the effects of other factors such as alcohol consumption related to antisocial behavior is not completely understood.

Methods: This study examines the conjunct effect of MAOA‐LPR, alcohol consumption, and aging on the risk for violent behavior. Recidivism in severe impulsive violent behavior was assessed after 7 to 15 years in a sample of 174 Finnish alcoholic offenders, the majority of whom exhibited antisocial or borderline personality disorder or both, and featured impulsive temperament traits.

Results: The risk for committing new acts of violence increased by 2.3% for each kilogram of increase in yearly mean alcohol consumption (p = 0.004) and decreased by 7.3% for every year among offenders carrying the high activity MAOA genotype. In contrast, alcohol consumption and aging failed to affect violent behavior in the low activity MAOA genotyped offenders. MAOA‐LPR showed no main effect on the risk for recidivistic violence.

Conclusions: Violent offenders carrying the high activity MAOA genotype differ in several ways from carriers with the low activity MAOA risk allele previously associated with antisocial behavior. Finnish high activity MAOA genotyped risk alcoholics exhibiting antisocial behavior, high alcohol consumption, and abnormal alcohol‐related impulsive and uncontrolled violence might represent an etiologically distinct alcohol dependence subtype.

Number of times cited: 32

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