Thursday, March 10, 2016

Genetic Background of Extreme Violent Behavior

In developed countries, the majority of all violent crime is committed by a small group of antisocial recidivistic offenders, but no genes have been shown to contribute to recidivistic violent offending or severe violent behavior, such as homicide. 

Our results, from two independent cohorts of Finnish prisoners, revealed that a monoamine oxidase A (MAOA) low-activity genotype (contributing to low dopamine turnover rate) as well as the CDH13 gene (coding for neuronal membrane adhesion protein) are associated with extremely violent behavior (at least 10 committed homicides, attempted homicides or batteries). No substantial signal was observed for either MAOA or CDH13 among non-violent offenders, indicating that findings were specific for violent offending, and not largely attributable to substance abuse or antisocial personality disorder. 

These results indicate both low monoamine metabolism and neuronal membrane dysfunction as plausible factors in the etiology of extreme criminal violent behavior, and imply that at least about 5–10% of all severe violent crime in Finland is attributable to the aforementioned MAOA and CDH13 genotypes.

Below:  Age- and gender-adjusted odds ratios for low-activity MAOA genotype and CDH13 (rs11649622) as a function of the number of committed violent crimes. The number of individuals, allele frequencies and odds ratios are shown below. The number of control subjects was 1946 for MAOA and 1877 for CDH13 analysis.

Below:  Manhattan plot of extremely violent offenders GWAS. The highest cluster is seen in locus 16q23.3

Full article at:

1Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
2Department of Forensic Psychiatry, University of Eastern Finland, Niuvanniemi Hospital, Kuopio, Finland
3National Institute for Health and Welfare, Helsinki, Finland
4Stanford University Center for Sleep Sciences, Palo Alto, CA, USA
5Department of Psychiatry, University of Helsinki, Institute of Clinical Medicine, Helsinki, Finland
6Department of Psychiatry, Helsinki University Central Hospital, Helsinki, Finland
7Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, England
8Analytic and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
9Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA
10Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland
11Psychiatric & Neurodevelopmental Genetics Unit, Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA
12Social Psychiatry Unit, School of Health Sciences, University of Tampere, Finland
13Psychiatric Hospital for Prisoners, Turku, Finland
14University of Turku, Turku, Finland
15Finnish Genome Center, Helsinki, Finland
16The Criminal Sanctions Agency, Helsinki, Finland
17University of Eastern Finland, Bioinformatics Center, Kuopio, Finland
18Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD, USA
Correspondence: Professor J Tiihonen, Karolinska Institutet, Department of Clinical Neuroscience, Byggnad R5, Stockholm, S-171 76, Sweden or Professor T Paunio, National Institute for Health and Welfare, PO Box 30, FI-00271, Finland.  es.ik@nenohiit.iraj or ; if.lht@oinuap.aniit
19These authors contributed equaliy to this work.
Mol Psychiatry. Author manuscript; available in PMC 2016 Mar 3. Mol Psychiatry. 2015 Jun; 20(6): 786–792.

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