Parental and perinatal risk factors for sexual offending in men: a nationwide case-control study.

BACKGROUND: Prior studies suggest parental and perinatal risk factors are associated with later offending. It remains uncertain, however, if such risk factors are similarly related to sexual offending. METHOD: We linked socio-demographic, family relations, and perinatal (obtained at birth) data from the nationwide Swedish registers from 1973 to 2009 with information on criminal convictions of cases and control subjects. Male sex offenders (n = 13 773) were matched 1:5 on birth year and county of birth in Sweden to male controls without sexual or non-sexual violent convictions. To examine risk-factor specificity for sexual offending, we also compared male violent, non-sexual offenders (n = 135 953) to controls without sexual or non-sexual violent convictions. Predictors included parental (young maternal or paternal age at son's birth, educational attainment, violent crime, psychiatric disorder, substance misuse, suicide attempt) and perinatal (number of older brothers, low Apgar score, low birth weight, being small for gestational age, congenital malformations, small head size) variables. RESULTS: Conditional logistic regression models found consistent patterns of statistically significant, small to moderate independent associations of parental risk factors with sons' sexual offending and non-sexual violent offending. For perinatal risk factors, patterns varied more; small for gestational age and small head size exhibited similar risk effects for both offence types whereas a higher number of older biological brothers and any congenital malformation were small, independent risk factors only for non-sexual violence. CONCLUSIONS: This nationwide study suggests substantial commonalities in parental and perinatal risk factors for the onset of sexual and non-sexual violent offending.

Schizophrenia and subsequent neighborhood deprivation: revisiting the social drift hypothesis using population, twin and molecular genetic data.

Neighborhood influences in the etiology of schizophrenia have been emphasized in a number of systematic reviews, but causality remains uncertain. To test the social drift hypothesis, we used three complementary genetically informed Swedish cohorts. First, we used nationwide Swedish data on approximately 760 000 full- and half-sibling pairs born between 1951 and 1974 and quantitative genetic models to study genetic and environmental influences on the overlap between schizophrenia in young adulthood and subsequent residence in socioeconomically deprived neighborhoods. Schizophrenia diagnoses were ascertained using the National Patient Registry. Second, we tested the overlap between childhood psychotic experiences and neighborhood deprivation in early adulthood in the longitudinal Twin Study of Child and Adolescent Development (TCHAD; n=2960). Third, we investigated to what extent polygenic risk scores for schizophrenia predicted residence in deprived neighborhoods during late adulthood using the TwinGene sample (n=6796). Sibling data suggested that living in deprived neighborhoods was substantially heritable; 65% (95% confidence interval (95% CI): 60-71%) of the variance was attributed to genetic influences. Although the correlation between schizophrenia and neighborhood deprivation was moderate in magnitude (r=0.22; 95% CI: 0.20-0.24), it was entirely explained by genetic influences. We replicated these findings in the TCHAD sample. Moreover, the association between polygenic risk for schizophrenia and neighborhood deprivation was statistically significant (R(2)=0.15%, P=0.002). Our findings are primarily consistent with a genetic selection interpretation where genetic liability for schizophrenia also predicts subsequent residence in socioeconomically deprived neighborhoods. Previous studies may have overemphasized the relative importance of environmental influences in the social drift of schizophrenia patients. Clinical and policy interventions will therefore benefit from the future identification of potentially causal pathways between different dimensions of cognitive functions and socioeconomic trajectories derived from studies adopting family-based research designs.

Age-specific suicide mortality following non-fatal self-harm: national cohort study in Sweden.

BACKGROUND: Possible age-related differences in risk of completed suicide following non-fatal self-harm remain unexplored. We examined associations between self-harm and completed suicide across age groups of self-harming patients, and whether these associations varied by violent index method, presence of mental disorder, and repeated self-harm. METHOD: The design was a cohort study with linked national registers in Sweden. The study population comprised individuals aged ⩾10 years hospitalized during 1990-1999 due to non-fatal self-harm (n = 53 843; 58% females) who were followed for 9-19 years. We computed hazard ratios (HRs) across age groups (age at index self-harm episode), with time to completed suicide as outcome. RESULTS: The 1-year HR for suicide among younger males (10-19 years) was 14.6 [95% confidence interval (CI) 4.1-51.9] for violent method and 8.4 (95% CI 1.8-40.0) for mental disorder. By contrast, none of the three potential risk factors increased the 1-year risks in the youngest females. Among patients aged ⩾20 years, the 1-year HR for violent method was 4.6 (95% CI 3.8-5.4) for males and 10.4 (95% CI 8.3-13.0) for females. HRs for repeated self-harm during years 2-9 of follow-up were higher in 10- to 19-year-olds (males: HR 4.0, 95% CI 2.0-7.8; females: HR 3.7, 95% CI 2.1-6.5). The ⩾20 years age groups had higher HRs than the youngest, particularly for females and especially within 1 year. CONCLUSIONS: Violent method and mental disorder increase the 1-year suicide risk in young male self-harm patients. Further, violent method increases suicide risk within 1 year in all age and gender groups except the youngest females. Repeated self-harm may increase the long-term risk more in young patients. These aspects should be accounted for in clinical suicide risk assessment.

Offspring psychopathology following preconception, prenatal and postnatal maternal bereavement stress.

BACKGROUND: Preconception, prenatal and postnatal maternal stress is associated with increased offspring psychopathology, but findings are inconsistent and need replication. We estimated associations between maternal bereavement stress and offspring autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), bipolar disorder, schizophrenia, suicide attempt and completed suicide. METHOD: Using Swedish registers, we conducted the largest population-based study to date examining associations between stress exposure in 738,144 offspring born 1992-2000 for childhood outcomes and 2,155,221 offspring born 1973-1997 for adult outcomes with follow-up to 2009. Maternal stress was defined as death of a first-degree relative during (a) the 6 months before conception, (b) pregnancy or (c) the first two postnatal years. Cox proportional survival analyses were used to obtain hazard ratios (HRs) in unadjusted and adjusted analyses. RESULTS: Marginal increased risk of bipolar disorder and schizophrenia following preconception bereavement stress was not significant. Third-trimester prenatal stress increased the risk of ASD [adjusted HR (aHR) 1.58, 95% confidence interval (CI) 1.15-2.17] and ADHD (aHR 1.31, 95% CI 1.04-1.66). First postnatal year stress increased the risk of offspring suicide attempt (aHR 1.13, 95% CI 1.02-1.25) and completed suicide (aHR 1.51, 95% CI 1.08-2.11). Bereavement stress during the second postnatal year increased the risk of ASD (aHR 1.30, 95% CI 1.09-1.55). CONCLUSIONS: Further research is needed regarding associations between preconception stress and psychopathological outcomes. Prenatal bereavement stress increases the risk of offspring ASD and ADHD. Postnatal bereavement stress moderately increases the risk of offspring suicide attempt, completed suicide and ASD. Smaller previous studies may have overestimated associations between early stress and psychopathological outcomes.

A Swedish national adoption study of criminality.

BACKGROUND: To clarify the role of genetic and environmental factors in criminal behavior (CB), we examined all CB and violent and non-violent subtypes (VCB and NVCB, respectively) in a Swedish national sample of adoptees and their relatives. METHOD: CB was defined by a conviction in the Swedish Crime Register with standard definitions for VCB and NVCB subtypes. We examined adoptees born 1950-1991 (n = 18 070) and their biological (n = 79 206) and adoptive (n = 47 311) relatives. RESULTS: The risk for all CB was significantly elevated in the adopted-away offspring of biological parents of which at least one had CB [odds ratio (OR) 1.5, 95% confidence interval (CI) 1.4-1.6] and in the biological full and half-siblings of CB adoptees (OR 1.4, 95% CI 1.2-1.6 and OR 1.3, 95% CI 1.2-1.3, respectively). A genetic risk index (including biological parental/sibling history of CB and alcohol abuse) and an environmental risk index (including adoptive parental and sibling CB and a history of adoptive parental divorce, death, and medical illness) both strongly predicted probability of CB. These genetic and environmental risk indices acted additively on adoptee risk for CB. Moderate specificity was seen in the transmission of genetic risk for VCB and NVCB between biological parents and siblings and adoptees. CONCLUSIONS: CB is etiologically complex and influenced by a range of genetic risk factors including a specific liability to CB and a vulnerability to broader externalizing behaviors, and by features of the adoptive environment including parental CB, divorce and death. Genetic risk factors for VCB and NVCB may be at least partially distinct.

Offspring death and subsequent psychiatric morbidity in bereaved parents: addressing mechanisms in a total population cohort.

BACKGROUND: It is unclear if psychiatric morbidity among parents bereaved of a child is related to major loss in general or if the cause of death matters. Whether such a link is consistent with a causal explanation also remains uncertain. METHOD: We identified 3,114,564 parents through linkage of Swedish nationwide registers. Risk of psychiatric hospitalization was assessed with log-linear Poisson regression and family-based analyses were used to explore familial confounding. RESULTS: A total of 3284 suicides and 14,095 any-cause deaths were identified in offspring between 12 and 25 years of age. Parents exposed to offspring suicide had considerably higher risk of subsequent psychiatric hospitalization than unexposed parents [relative risk (RR) 1.90, 95% confidence interval (CI) 1.72-2.09], higher than parents exposed to offspring non-suicide death relative to controls (RR 1.18, 95% CI 1.11-1.26). We found no risk increase among stepfathers differentially exposed to biologically unrelated stepchildren's death or suicide, and the relative risk was notably lower among full siblings differentially exposed to offspring death or suicide. CONCLUSIONS: Parental psychiatric hospitalization following offspring death was primarily found in offspring suicide. Familial (e.g. shared genetic) effects seemed important, judging from both lack of psychiatric hospitalization in bereaved stepfathers and attenuated risk when bereaved parents were contrasted to their non-bereaved siblings. We conclude that offspring suicide does not 'cause' psychiatric hospitalization in bereaved parents.

Stimulant and non-stimulant attention deficit/hyperactivity disorder drug use: total population study of trends and discontinuation patterns 2006-2009.

OBJECTIVE: To explore the prevalence and discontinuation of dispensed medications for attention deficit/hyperactivity disorder (ADHD) drugs from 2006 to 2009. METHOD: A total population cohort of all individuals aged 6-45 years, alive and registered as residents in Sweden during any calendar year from 2006 to 2009 (N = 5 149 791) included 41 700 patients dispensed with an ADHD drug (methylphenidate, atomoxetine, amphetamine, or dexamphetamine). The dispensing prevalence was calculated for each year, stratified on sex and age. A longitudinal analysis was also performed to compare the rates of treatment discontinuation across the strata. RESULTS: The dispensing prevalence increased from 2.93 per 1000 in 2006 to 6.98 in 2009 (PR = 2.38, 95% CI = 2.34-2.43). The prevalence ratio (PR) was 3.40 for adults, 22-45 years old; 2.41 for adolescents, 15-21 years old; and 1.90 for children aged 6-14. The increase was also greater in women than in men (PR = 2.92 vs. 2.19). Patients aged 15-21 were the most likely to discontinue treatment; after 3 years and 11 months, 27% of those patients were still under treatment. CONCLUSION: From 2006 to 2009, the number of prescriptions dispensed for ADHD drugs increased substantially. The rate of treatment discontinuation in the age interval 15-21 is higher than expected considering the persistence rates of the disorder.

Parental schizophrenia and increased offspring suicide risk: exploring the causal hypothesis using cousin comparisons.

BACKGROUND: Little is known about suicide risk among offspring of parents hospitalized for schizophrenia and the mechanisms behind this association. METHOD: We applied a nested case-control design based on linkage of Swedish population-based registers. Among 12- to 30-year-old offspring, we identified 68 318 offspring with suicidal behavior (attempted and completed suicide) and their parents. Five healthy control-parent pairs were matched to each suicidal case-parent pair and conditional logistic regression used to obtain odds ratios (ORs). Further, to disentangle familial confounding from causal environmental mechanisms, we compared the population-based suicide risk with the risk found within full-cousins and half-cousins differentially exposed to parental schizophrenia. RESULTS: Offspring of parents with schizophrenia had significantly increased suicide risk after accounting for socio-economic status, parental suicidal behavior and offspring mental illness [OR 1.68, 95% confidence interval (CI) 1.53-1.85]. Suicide risks in offspring of schizophrenic mothers and fathers were similar in magnitude; so were risks across different developmental periods. Importantly, offspring suicide risk remained essentially unchanged across genetically different relationships; offspring of siblings discordant for schizophrenia had equivalent risk increases within full-cousins (OR 1.96, 95% CI 1.66-2.31) and half-cousins (OR 1.69, 95% CI 1.17-2.44). CONCLUSIONS: Parental schizophrenia was associated with increased risk of offspring suicidal behavior, independent of gender of the schizophrenic parent, and persisting into adulthood. The suicide risk in offspring remained at a similar level when comparing genetically different relationships, which suggests that at least part of the association is due to environmental mechanisms. These findings should inspire increased attention to suicidal ideation and prevention efforts in offspring of parents with schizophrenia.

Child maltreatment and adult violent offending: population-based twin study addressing the 'cycle of violence' hypothesis.

BACKGROUND: Associations between child maltreatment and adult violence, often termed the 'cycle of violence', are well documented. However, the nature of such links after appropriate control for confounding remains uncertain. We aimed to determine whether child maltreatment causes adult violent offending or whether suggested links are due to genetic or family environment confounding. METHOD: A total of 18 083 20- to 47-year-old twins from the Swedish population-based Study of Twin Adults: Genes and Environment (STAGE) participated. We linked information on self-reported child maltreatment with national register data on convictions for adult crime. We used a case-control design to elucidate associations among unrelated individuals and also conducted within-discordant twin pair analyses to estimate the influence of familial confounding on this association. RESULTS: The odds ratio (OR), adjusted for age, sex and education, for violent offending in maltreated children grown up versus unrelated controls was 1.98 [95% confidence interval (CI) 1.52-2.57]. However, the association decreased to 1.18 (95% CI 0.62-2.25) when maltreated children were compared to their non-maltreated twins, suggesting substantial confounding by genetic or family environmental factors (within-twin OR<1.98) and a weak, non-significant causal effect (within-twin OR>1.00). Familial confounding was also pronounced for the association between child maltreatment and any offending. CONCLUSIONS: Childhood maltreatment was found to be a weak causal risk factor for adult violent offending; hence, reducing maltreatment might decrease violent crime less than previously expected. Instead, considerable familial confounding of the link between child maltreatment and adult violent offending suggests that prevention strategies need to address overlapping genetic and/or family environmental liability for abusive and violent behavior.

Disentangling the relationships between maternal smoking during pregnancy and co-occurring risk factors.

BACKGROUND: Maternal smoking during pregnancy (SDP) has been studied extensively as a risk factor for adverse offspring outcomes and is known to co-occur with other familial risk factors. Accounting for general familial risk factors has attenuated associations between SDP and adverse offspring outcomes, and identifying these confounds will be crucial to elucidating the relationship between SDP and its psychological correlates. METHOD: The current study aimed to disentangle the relationship between maternal SDP and co-occurring risk factors (maternal criminal activity, drug problems, teen pregnancy, educational attainment, and cohabitation at childbirth) using a population-based sample of full- (n=206 313) and half-sister pairs (n=19 363) from Sweden. Logistic regression models estimated the strength of association between SDP and co-occurring risk factors. Bivariate behavioral genetic models estimated the degree to which associations between SDP and co-occurring risk factors are attributable to genetic and environmental factors. RESULTS: Maternal SDP was associated with an increase in all co-occurring risk factors. Of the variance associated with SDP, 45% was attributed to genetic factors and 53% was attributed to unshared environmental factors. In bivariate models, genetic factors accounted for 21% (non-drug-, non-violence-related crimes) to 35% (drug-related crimes) of the covariance between SDP and co-occurring risk factors. Unshared environmental factors accounted for the remaining covariance. CONCLUSIONS: The genetic factors that influence a woman's criminal behavior, substance abuse and her offspring's rearing environment all influence SDP. Therefore, the intergenerational transmission of genes conferring risk for antisocial behavior and substance misuse may influence the associations between maternal SDP and adverse offspring outcomes.

Poor school performance in offspring of patients with schizophrenia: what are the mechanisms?

BACKGROUND: Offspring of patients with schizophrenia exhibit poorer school performance compared with offspring of non-schizophrenic parents. We aimed to elucidate the mechanisms behind this association. METHOD: We linked longitudinal national population registers in Sweden and compared school performance among offspring of schizophrenic parents with offspring of non-schizophrenic parents (1 439 215 individuals with final grades from compulsory school 1988-2006). To investigate the mechanisms, we studied offspring of schizophrenic patients and controls within the same extended families. We investigated genetic effects by stratifying analyses of parent-child associations according to genetic relatedness (half-cousins, full cousins and half-siblings). Environmental effects were investigated by comparing school performance of offspring of schizophrenic fathers and of schizophrenic mothers, respectively, and by stratifying the analyses according to environmental relatedness while controlling genetic relatedness (paternal and maternal half-cousins, paternal and maternal half-siblings). RESULTS: Offspring of parents with schizophrenia had poorer overall school performance than unrelated offspring of non-schizophrenic parents (-0.31 s.d.). Variability in genetic relatedness greatly moderated the strength of the within-family association (ß=-0.23 within exposure-discordant half-cousins, ß=-0.13 within exposure-discordant full cousins, ß=0.04 within exposure-discordant half-siblings), while no evidence was found that the environment affected offspring school performance. CONCLUSIONS: Genetic factors account for poorer school performance in children of parents with schizophrenia. This supports that cognitive deficits found in individuals with schizophrenia and their relatives might be genetically inherited. Early detection of prodromal signs and impaired functioning of offspring of patients with schizophrenia could lead to earlier and better tailored interventions.

Validity of bipolar disorder hospital discharge diagnoses: file review and multiple register linkage in Sweden.

OBJECTIVE: Hospital discharge registers (HDRs) are frequently used in epidemiological research. However, the validity of several important psychiatric diagnostic entities, including bipolar disorder, remains uncertain. Hence, we aimed to develop an optimal algorithm for register-based identification of DSM-IV-TR bipolar disorder. METHOD: We identified potential cases in the Swedish national HDR using two separate discharge diagnoses of bipolar disorder according to ICD versions 8-10 during January 1, 1973 to December 31, 2004. In a randomly selected subsample of 135 cases from the county of Sörmland, two senior psychiatrists reassessed the diagnostic status based on patients' medical records. We scrutinized false-positive cases and modified the initial algorithm to improve positive predictive value while minimizing false negatives. Finally, we externally validated resulting caseness algorithms by linking HDR diagnostic data with best-estimate clinical diagnoses from the National Quality Assurance Register for Bipolar Disorder (BipoläR), dispensed lithium prescriptions from the National Prescribed Drug Register, and the ICD-10 diagnoses from the National Outpatient Register respectively. RESULTS: The algorithm with two discharge diagnoses of bipolar disorder yielded a positive predictive value of 0.81. Modification by excluding individuals diagnosed with ICD-8 296.20 (manic-depressive psychosis, depressed type), and/or ICD-9 296.B (unipolar affective psychosis, melancholic form), gave a positive positive predictive value of 0.92. The modified algorithm also had statistically superior external validity compared with the original algorithm. CONCLUSION: Our findings suggest that DSM-IV-TR bipolar disorder caseness based on two inpatient episodes with a bipolar disorder diagnosis is sufficiently sensitive and specific to be used in further epidemiological study of bipolar disorder.

Familial clustering of suicide risk: a total population study of 11.4 million individuals.

BACKGROUND: Research suggests that suicidal behaviour is aggregated in families. However, due to methodological limitations, including small sample sizes, the strength and pattern of this aggregation remains uncertain. METHOD: We examined the familial clustering of completed suicide in a Swedish total population sample. We linked the Cause of Death and Multi-Generation Registers and compared suicide rates among relatives of all 83 951 suicide decedents from 1952-2003 with those among relatives of population controls. RESULTS: Patterns of familial aggregation of suicide among relatives to suicide decedents suggested genetic influences on suicide risk; the risk among full siblings (odds ratio 3.1, 95% confidence interval 2.8-3.5, 50% genetic similarity) was higher than that for maternal half-siblings (1.7, 1.1-2.7, 25% genetic similarity), despite similar environmental exposure. Further, monozygotic twins (100% genetic similarity) had a higher risk than dizygotic twins (50% genetic similarity) and cousins (12.5% genetic similarity) had higher suicide risk than controls. Shared (familial) environmental influences were also indicated; siblings to suicide decedents had a higher risk than offspring (both 50% genetically identical but siblings having a more shared environment, 3.1, 2.8-3.5 v. 2.0, 1.9-2.2), and maternal half-siblings had a higher risk than paternal half-siblings (both 50% genetically identical but the former with a more shared environment). Although comparisons of twins and half-siblings had overlapping confidence intervals, they were supported by sensitivity analyses, also including suicide attempts. CONCLUSIONS: Familial clustering of suicide is primarily influenced by genetic and also shared environmental factors. The family history of suicide should be considered when assessing suicide risk in clinical settings or designing and administering preventive interventions.

Violent crime runs in families: a total population study of 12.5 million individuals.

BACKGROUND: Etiological theory and prior research with small or selected samples suggest that interpersonal violence clusters in families. However, the strength and pattern of this aggregation remains mostly unknown. METHOD: We investigated all convictions for violent crime in Sweden 1973-2004 among more than 12.5 million individuals in the nationwide Multi-Generation Register, and compared rates of violent convictions among relatives of violent individuals with relatives of matched, non-violent controls, using a nested case-control design. RESULTS: We found strong familial aggregation of interpersonal violence among first-degree relatives [e.g. odds ratio (OR)sibling 4.3, 95% confidence interval (CI) 4.2-4.3], lower for more distant relatives (e.g. OR cousin 1.9, 95% CI 1.9-1.9). Risk patterns across biological and adoptive relations provided evidence for both genetic and environmental influences on the development of violent behavior. Familial risks were stronger among women, in higher socio-economic strata, and for early onset interpersonal violence. There were crime-specific effects (e.g. OR sibling for arson 22.4, 95% CI 12.2-41.2), suggesting both general and subtype-specific familial risk factors for violent behavior. CONCLUSIONS: The observed familiality should be accounted for in criminological research, applied violence risk assessment, and prevention efforts.

Psychiatric morbidity associated with same-sex sexual behaviour: influence of minority stress and familial factors.

BACKGROUND: Increased psychiatric morbidity has been widely reported among non-heterosexual individuals (defined as reporting a homosexual/bisexual identity and/or same-sex sexual partners). However, the causes of this psychiatric ill-health are mostly unknown. METHOD: We attempted to estimate the influence of minority stress and familial factors on psychiatric disorder among adults with same-sex sexual partners. Self-report data from a 2005 survey of adults (age 20-47 years, n=17,379) in the population-based Swedish Twin Registry were analysed with regression modelling and co-twin control methodology. RESULTS: Rates of depression, generalized anxiety disorder (GAD), eating disorders, alcohol dependence and attention deficit hyperactivity disorder (ADHD) were increased among men and women with same-sex sexual experiences. Adjusting for perceived discrimination and hate crime victimization lowered this risk whereas controlling for familial (genetic or environmental) factors in within-twin pair comparisons further reduced or eliminated it. CONCLUSIONS: Components of minority stress influence the risk of psychiatric ill-health among individuals with any same-sex sexual partner. However, substantial confounding by familial factors suggests a common genetic and/or environmental liability for same-sex sexual behaviour and psychiatric morbidity.

Psychopathy and violent recidivism among young criminal offenders.

OBJECTIVE: To investigate the predictive validity of psychopathic personality traits (assessed with the revised psychopathy checklist, PCL-R; Hare, 1991) for violent criminal recidivism among young offenders. METHOD: The relationship between PCL-R psychopathy and violent re-offending was studied in 98 young (M=18.40, range 15-20 years) violent and sex offenders subjected to forensic psychiatric evaluation in Sweden during 1988-95. Subjects were followed during detainment and for 24 months in the community to first reconviction for a violent offence. RESULTS: We found a modest but significant association between PCL-R scores and violent recidivism, almost exclusively accounted for by behavioural criteria. Among 13 possible confounders tested, conduct disorder before age 15 and a young age at first conviction eliminated the relationship between psychopathy and violent recidivism in pair-wise logistic regression models. CONCLUSION: PCL-R psychopathy may be a less valid predictor for violent criminal recidivism among severe youthful offenders than among adult offenders.

Actuarial assessment of sex offender recidivism risk: a cross-validation of the RRASOR and the Static-99 in Sweden.

We cross-validated two actuarial risk assessment tools, the RRASOR (R. K. Hanson, 1997) and the Static-99 (R. K. Hanson & D. Thornton, 1999), in a retrospective follow-up (mean follow-up time = 3.69 years) of all sex offenders released from Swedish prisons during 1993-1997 (N = 1,400, all men, age > or =18 years). File-based data were collected by a researcher blind to the outcome (registered criminal recidivism), and individual risk factors as well as complete instrument characteristics were explored. Both the RRASOR and the Static-99 showed similar and moderate predictive accuracy for sexual reconvictions whereas the Static-99 exhibited a significantly higher accuracy for the prediction of any violent recidivism as compared to the RRASOR. Although particularly the Static-99 proved moderately robust as an actuarial measure of recidivism risk among sexual offenders in Sweden, both procedures may need further evaluation, for example, with sex offender subpopulations differing ethnically or with respect to offense characteristics. The usefulness of actuarial methods for the assessment of sex offender recidivism risk is discussed in the context of current practice.

A preliminary typology of young sex offenders.

Data concerning all young (15-20 years, n = 56) sex offenders (YSOs) subjected to forensic psychiatric investigation in Sweden during 1988-1995 were used in an attempt to construct and validate an introductory YSO typology based solely on offence characteristics. A 5-cluster solution received optimal support from cluster analysis of 15 offence-related variables. A few historical and clinical characteristics varied across clusters. Survival analyses revealed that the clusters differed with respect to sexual but not to violent or general reconviction rates.

Psychopathy (PCL-R) as a predictor of violent recidivism among criminal offenders with schizophrenia.

Hare's Psychopathy Checklist--Revised (PCL-R) was used to test the hypothesis that psychopathy predicts violent recidivism in a cohort subjected to forensic psychiatric investigation and consisting of male violent offenders with schizophrenia (N = 202). Psychopathy was assessed with retrospective file-based ratings. Mean follow-up time after detainment was 51 months. Twenty-two percent of the offenders had a PCL-R score > or = 26 (cutoff), and the base rate for violent recidivism (reconvictions) during follow-up was 21%. Survival analysis revealed that psychopathy was strongly associated to violent recidivism (log-rank = 17.71, df = 1, p < 0.0001). The area under the curve (AUC) of the receiver operating characteristics (ROC) of PCL-R total score to predict violent recidivism varied between different time frames from .64 to .75. Cox regression analyses revealed that other potential risk factors could not equally well or better explain violent recidivism in the cohort than psychopathy as measured by PCL-R.

The medico-legal status of young sex offenders: forensic psychiatric evaluations in Sweden 1988-1995.

Young sex offenders (YSOs) attract significant public and professional concern. YSOs might be perceived as more psychologically deviant or dangerous than other offenders. This study focused on how often YSOs subjected to forensic psychiatric investigation (FPI) were declared medico-legally insane as compared to young non-sex offenders and adult sex offenders. Logistic regression models were applied to data from all major FPIs performed in Sweden between 1988 and 1995 (N=4354) to explore factors affecting the likelihood of receiving a medico-legal insanity declaration. When we adjusted for the statistical effects of age, sex offender status, and psychopathology, YSOs (n=47) were three to four times more likely to be declared insane in the medico-legal sense. The results indicate that YSOs in Sweden constitute a medico-legally distinct subgroup of forensic psychiatric examinees.