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.

Psychopathy is an extreme form of antisocial behavior, with about 1% prevalence in the general population, and 10-30% among incarcerated criminal offenders. Although the heritability of severe antisocial behavior is up to 50%, the genetic background is unclear. The underlying molecular mechanisms have remained unknown but several previous studies suggest that abnormal glucose metabolism and opioidergic neurotransmission contribute to violent offending and psychopathy. Here we show using iPSC-derived cortical neurons and astrocytes from six incarcerated extremely antisocial and violent offenders, three nonpsychopathic individuals with substance abuse, and six healthy controls that there are robust alterations in the expression of several genes and immune response-related molecular pathways which were specific for psychopathy. In neurons, psychopathy was associated with marked upregulation of RPL10P9 and ZNF132, and downregulation of CDH5 and OPRD1. In astrocytes, RPL10P9 and MT-RNR2 were upregulated. Expression of aforementioned genes explained 30-92% of the variance of psychopathic symptoms. The gene expression findings were confirmed with qPCR. These genes may be relevant to the lack of empathy and emotional callousness seen in psychopathy, since several studies have linked these genes to autism and social interaction.

The PCL-R is a reliable and valid measure of the psychopathy construct of the Finnish male prisoners. The PCL-R is applicable to the Finnish offenders and it is a useful tool for assessing psychopathy in the Finnish criminal justice settings.

Assessing and targeting substance abuse-related treatment needs according to evidence-based practice has become the norm in most prison administrations. Not everyone with a need will, however, receive support in practical settings. Drawing on Finnish prison registers, we show that of all prisoners released in 2011, 60% were assessed as having a need for substance abuse-related support. Of these, 22% received an intervention in prison. Two multivariate models were used to examine the factors related to selection into interventions. The main factors associated with receiving an intervention with evidence-based programmes were a longer sentence, Finnish nationality, younger age and treatment motivation. The predictors for any substance abuse interventions (including non-evidence-based) were the same, with the exception that motivation was no longer a significant predictor, and female gender remained significant. The selective use of motivation as an entrance criterion for interventions can be a means of systemic adaptation to a combination of a high prevalence of substance abuse problems and a lower prevalence of treatment motivation in the prison population. We discuss how our results might reflect a Scandinavian way of doing evidence-based, prison-based drug treatment-one that stresses rehabilitation as a goal in itself in addition to reducing recidivism. Most prisoners, however, do not receive any intervention at all.

Substance abuse is viewed as one of the main factors (criminogenic needs) to be assessed and targeted in prison. Prison assessments of risk and needs are known to validly predict reoffending. However, there seems to be lacking research in how reliably the individual prisoner's problems, such as substance abuse, are represented in the assessments. In this study, we compare an independent medical health study (N=510) with in-prison assessments for the Eur J Crim Policy Res same persons to see whether some of the inmates' substance abuse disorders were overlooked in prison. We found that sentence plans (257) were in poor agreement with the health study (Kappa 0.315); they recognized only 65 % of all diagnoses. The risk and needs assessments (178) were in closer agreement with the health study, however, alcoholism diagnoses were recognized less accurately (Kappa 0.519) and less frequently (78 %) than drug diagnoses (Kappa 0.627, 87 %). The main factors predicting an assessment of substance abuse risks in prison, analysed through logistic regression were: longer stay in prison and one or more dependence diagnoses. We conclude that, a number of potentially criminogenic dependence problems remain unrecognized since some groups of prisoners are either completely left out from the more thorough instrument, the risk-and-needs assessment, or are not assessed thoroughly enough. This puts prisoners in unequal positions, since all interventions in prison are based on assessments. The study alerts us of the selectiveness of prisoner assessments in practical settings; the unrecognition of problems of shorter sentenced prisoners and prisoners with alcohol dependence.