Paul Lichtenstein

University of Oxford, Oxford, England, United Kingdom

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Publications (467)3180.04 Total impact

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    ABSTRACT: Emerging evidence suggests that physical activity (PA) enhances cognition and may be a protective factor for attention-deficit/hyperactivity disorder (ADHD). Yet the impact of PA on ADHD symptoms has been investigated only in a few undersized, nonrandomized, and retrospective studies. We examined the effect of PA during late adolescence on ADHD symptoms in early adulthood while controlling for unmeasured genetic and shared environmental confounding. The effect of PA at age 16 to 17 years (baseline) on ADHD symptoms at age 19 to 20 years (follow-up) was examined using a within-monozygotic (MZ) twins fixed-effects model in 232 MZ twin pairs born in Sweden between May 1985 and December 1986. Parents rated their children's DSM ADHD symptoms at baseline and follow-up. Participants' weekly energy expenditure (in metabolic equivalent task minutes per week) was based on self-reports at baseline of PA frequency, intensity, and duration. Greater weekly energy expenditure in adolescence was significantly associated with reduced ADHD symptom levels in early adulthood, even when controlling for unmeasured confounding (all genetic and environmental factors shared within MZ twin pairs) as well as ADHD symptoms and body mass index (BMI) at baseline, β = -0.21, p = .013 (95% CI = -0.38 to -0.05). Similar results were observed for the 2 ADHD subcomponents: hyperactivity/impulsivity, β = -0.21, p = .022 (95% CI = -0.39 to -0.03), and inattention, β = -0.19, p = .049 (95% CI = -0.36 to -0.0005). In line with a causal hypothesis, PA was inversely associated with ADHD symptoms, even after adjusting for unmeasured confounding. These findings suggest that PA in adolescence might decrease ADHD symptoms in early adulthood. However, given the size of the effect, the clinical value of this intervention needs to be explored further. Copyright © 2015 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.
    Journal of the American Academy of Child & Adolescent Psychiatry 07/2015; 54(7):565–570. DOI:10.1016/j.jaac.2015.04.011 · 6.35 Impact Factor
  • Seena Fazel, Guy M Goodwin, Paul Lichtenstein
    The Lancet Psychiatry 06/2015; 2(6). DOI:10.1016/S2215-0366(15)00225-4
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    ABSTRACT: Objectives The usefulness of cases diagnosed in administrative registers for research purposes is dependent on diagnostic validity. This study aimed to investigate the validity and inter-rater reliability of recorded diagnoses of tic disorders and obsessive-compulsive disorder (OCD) in the Swedish National Patient Register (NPR). Design Chart review of randomly selected register cases and controls. Method 100 tic disorder cases and 100 OCD cases were randomly selected from the NPR based on codes from the International Classification of Diseases (ICD) 8th, 9th and 10th editions, together with 50 epilepsy and 50 depression control cases. The obtained psychiatric records were blindly assessed by 2 senior psychiatrists according to the criteria of the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) and ICD-10. Primary outcome measurement Positive predictive value (PPV; cases diagnosed correctly divided by the sum of true positives and false positives). Results Between 1969 and 2009, the NPR included 7286 tic disorder and 24 757 OCD cases. The vast majority (91.3% of tic cases and 80.1% of OCD cases) are coded with the most recent ICD version (ICD-10). For tic disorders, the PPV was high across all ICD versions (PPV=89% in ICD-8, 86% in ICD-9 and 97% in ICD-10). For OCD, only ICD-10 codes had high validity (PPV=91–96%). None of the epilepsy or depression control cases were wrongly diagnosed as having tic disorders or OCD, respectively. Inter-rater reliability was outstanding for both tic disorders (κ=1) and OCD (κ=0.98). Conclusions The validity and reliability of ICD codes for tic disorders and OCD in the Swedish NPR is generally high. We propose simple algorithms to further increase the confidence in the validity of these codes for epidemiological research.
    BMJ Open 06/2015; 5(6):e007520. DOI:10.1136/bmjopen-2014-007520 · 2.06 Impact Factor
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    ABSTRACT: Tic disorders, including Tourette syndrome (TS) and chronic tic disorders (CTDs), are assumed to be strongly familial and heritable. Although gene-searching efforts are well under way, precise estimates of familial risk and heritability are lacking. Previous controlled family studies were small and typically conducted within specialist clinics, resulting in potential ascertainment biases. They were also underpowered to disentangle genetic from environmental factors that contribute to the observed familiality. Twin studies have been either very small or based on parent-reported tics in population-based (nonclinical) twin samples. To provide unbiased estimates of familial risk and heritability of tic disorders at the population level. In this population cohort, multigenerational family study, we used a validated algorithm to identify 4826 individuals diagnosed as having TS or CTDs (76.2% male) in the Swedish National Patient Register from January 1, 1969, through December 31, 2009. We studied risks for TS or CTDs in all biological relatives of probands compared with relatives of unaffected individuals (matched on a 1:10 ratio) from the general population. Structural equation modeling was used to estimate the heritability of tic disorders. The risk for tic disorders among relatives of probands with tic disorders increased proportionally to the degree of genetic relatedness. The risks for first-degree relatives (odds ratio [OR], 18.69; 95% CI, 14.53-24.05) were significantly higher than for second-degree relatives (OR, 4.58; 95% CI, 3.22-6.52) and third-degree relatives (OR, 3.07; 95% CI, 2.08-4.51). First-degree relatives at similar genetic distances (eg, parents, siblings, and offspring) had similar risks for tic disorders despite different degrees of shared environment. The risks for full siblings (50% genetic similarity; OR, 17.68; 95% CI, 12.90-24.23) were significantly higher than those for maternal half siblings (25% genetic similarity; OR, 4.41; 95% CI, 2.24-8.67) despite similar environmental exposures. The heritability of tic disorders was estimated to be 0.77 (95% CI, 0.70-0.85). There were no differences in familial risk or heritability between male and female patients. Tic disorders, including TS and CTDs, cluster in families primarily because of genetic factors and appear to be among the most heritable neuropsychiatric conditions.
    JAMA Psychiatry 06/2015; DOI:10.1001/jamapsychiatry.2015.0627 · 12.01 Impact Factor
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    ABSTRACT: Prenatal exposure to air pollutants has been suggested as a possible etiologic factor for the occurrence of autism spectrum disorder. To assess whether prenatal air pollution exposure is associated with childhood autistic traits in the general population. Collaborative study of four European population-based birth/child cohorts -CATSS (Sweden), GENERATION R (the Netherlands), GASPII (Italy), and INMA (Spain). Nitrogen oxides (NO2, NOx) and particulate matter (PM) with diameters of <2.5 µm (PM2.5), <10 µm (PM10), and between 2.5-10 µm (PMcoarse) and PM2.5 absorbance- were estimated for birth addresses by land-use regression models based on monitoring campaigns performed between 2008 and 2011. Levels were extrapolated back in time to exact pregnancy periods. Autistic traits were assessed between four and ten years of age using quantitative assessments. Children were classified with autistic traits within the borderline/clinical range and within the clinical range using validated cut-offs. Adjusted cohort-specific effect estimates were combined using random-effects meta-analysis. A total of 8,079 children were included. Prenatal air pollution exposure was not associated with autistic traits within the borderline/clinical range (OR = 0.94; 95% CI: 0.81, 1.10 per each increase by 10 µg/m(3) in NO2 pregnancy levels). Similar results were observed in the different cohorts, for the other pollutants, and assessing children with autistic traits within the clinical range or children with autistic traits as a quantitative score. Prenatal exposure to NO2 and PM was not associated with autistic traits in children from four to ten years of age in four European population-based birth/child cohort studies.
    Environmental Health Perspectives 06/2015; DOI:10.1289/ehp.1408483 · 7.03 Impact Factor
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    ABSTRACT: To examine associations between varenicline and the incidence of a range of adverse outcomes. Population based cohort study using within person analyses to control for confounding by indication. Whole population of Sweden. 7 917 436 people aged 15 and over, of whom 69 757 were treated with varenicline between 2006 and 2009. Incidence of new psychiatric conditions, suicidal behaviour, suspected and convicted criminal offending, transport accidents, and suspected and convicted traffic offences. In the whole population, 337 393 new psychiatric conditions were diagnosed during follow-up. In addition, 507 823 suspected and 338 608 convicted crimes, 40 595 suicidal events, 124 445 transport accidents, and 99 895 suspected and 57 068 convicted traffic crimes were recorded. Within person analyses showed that varenicline was not associated with significant hazards of suicidal behaviour, criminal offending, transport accidents, traffic offences, or psychoses. However, varenicline was associated with a small increase in the risk of anxiety conditions (hazard ratio 1.23, 95% confidence interval 1.01 to 1.51) and mood conditions (1.31, 1.06 to 1.63), which was only seen in people with pre-existing psychiatric disorders. Concerns that varenicline is associated with an increased risk of many adverse outcomes, including suicidality and accidents, are not supported in this observational study. The small increase in risk of two psychiatric conditions in people with pre-existing psychiatric disorders needs to be confirmed using other research designs. © Molero et al 2015.
    BMJ (online) 06/2015; 350(jun02 2):h2388. DOI:10.1136/bmj.h2388 · 16.38 Impact Factor
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    ABSTRACT: For over 100 years, the genetics of human anthropometric traits has attracted scientific interest. In particular, height and body mass index (BMI, calculated as kg/m2) have been under intensive genetic research. However, it is still largely unknown whether and how heritability estimates vary between human populations. Opportunities to address this question have increased recently because of the establishment of many new twin cohorts and the increasing accumulation of data in established twin cohorts. We started a new research project to analyze systematically (1) the variation of heritability estimates of height, BMI and their trajectories over the life course between birth cohorts, ethnicities and countries, and (2) to study the effects of birth-related factors, education and smoking on these anthropometric traits and whether these effects vary between twin cohorts. We identified 67 twin projects, including both monozygotic (MZ) and dizygotic (DZ) twins, using various sources. We asked for individual level data on height and weight including repeated measurements, birth related traits, background variables, education and smoking. By the end of 2014, 48 projects participated. Together, we have 893,458 height and weight measures (52% females) from 434,723 twin individuals, including 201,192 complete twin pairs (40% monozygotic, 40% same-sex dizygotic and 20% opposite-sex dizygotic) representing 22 countries. This project demonstrates that large-scale international twin studies are feasible and can promote the use of existing data for novel research purposes.
    Twin Research and Human Genetics 05/2015; 10(10):1017. · 1.92 Impact Factor
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    ABSTRACT: Parental depressive symptoms are associated with emotional and behavioural problems in offspring. However, genetically informative studies are needed to distinguish potential causal effects from genetic confounds, and longitudinal studies are required to distinguish parent-to-child effects from child-to-parent effects. We conducted cross-sectional analyses on a sample of Swedish twins and their adolescent offspring (n = 876 twin families), and longitudinal analyses on a US sample of children adopted at birth, their adoptive parents, and their birth mothers (n = 361 adoptive families). Depressive symptoms were measured in parents, and externalizing and internalizing problems measured in offspring. Structural equation models were fitted to the data. Results of model fitting suggest that associations between parental depressive symptoms and offspring internalizing and externalizing problems remain after accounting for genes shared between parent and child. Genetic transmission was not evident in the twin study but was evident in the adoption study. In the longitudinal adoption study child-to-parent effects were evident. We interpret the results as demonstrating that associations between parental depressive symptoms and offspring emotional and behavioural problems are not solely attributable to shared genes, and that bidirectional effects may be present in intergenerational associations.
    Psychological Medicine 05/2015; DOI:10.1017/S0033291715000501 · 5.43 Impact Factor
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    ABSTRACT: We sought to clarify the etiological contribution of genetic and environmental factors to total criminal behavior (CB) measured as criminal convictions in men and women, and to violent (VCB), white-collar (WCCB) and property criminal behavior (PCB) in men only. In 21 603 twin pairs from the Swedish Twin Registry, we obtained information on all criminal convictions from 1973 to 2011 from the Swedish Crime Register. Twin modeling was performed using the OpenMx package. For all criminal convictions, heritability was estimated at around 45% in both sexes, with the shared environment accounting for 18% of the variance in liability in females and 27% in males. The correlation of these risk factors across sexes was estimated at +0.63. In men, the magnitudes of genetic and environmental influence were similar in the three criminal conviction subtypes. However, for violent and white-collar convictions, nearly half and one-third of the genetic effects were respectively unique to that criminal subtype. About half of the familial environmental effects were unique to property convictions. The familial aggregation of officially recorded CB is substantial and results from both genetic and familial environmental factors. These factors are moderately correlated across the sexes suggesting that some genetic and environmental influences on criminal convictions are unique to men and to women. Violent criminal behavior and property crime are substantially influenced respectively by genetic and shared environmental risk factors unique to that criminal subtype.
    Psychological Medicine 05/2015; DOI:10.1017/S0033291714002098 · 5.43 Impact Factor
  • Zheng Chang, Prof Paul Lichtenstein, Henrik Larsson, Seena Fazel
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    ABSTRACT: High mortality rates have been reported in people released from prison compared with the general population. However, few studies have investigated potential risk factors associated with these high rates, especially psychiatric determinants. We aimed to investigate the association between psychiatric disorders and mortality in people released from prison in Sweden.
    The Lancet Psychiatry 05/2015; 2(5):422-430. DOI:10.1016/S2215-0366(15)00088-7
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    ABSTRACT: Objective This study explored the cross-sectional and predictive effect of drive for thinness and/or negative affect scores on the development of self-reported anorexia nervosa (AN) and bulimia nervosa (BN).MethodK-means were used to cluster the Eating Disorder Inventory-Drive for Thinness (DT) and Child Behavior Checklist Anxious/Depressed (A/D) scores from 615 unrelated female twins at age 16–17. Logistic regressions were used to assess the effect of these clusters on self-reported eating disorder diagnosis at ages 16–17 (n = 565) and 19–20 (n = 451).ResultsDT and A/D scores were grouped into four clusters: Mild (scores lower than 90th percentile on both scales), DT (higher scores only on DT), A/D (higher scores only on A/D), and DT-A/D (higher scores on both the DT and A/D scales). DT and DT-A/D clusters at age 16–17 were associated cross-sectionally with AN and both cross-sectionally and longitudinally with BN. The DT-A/D cluster had the highest prevalence of AN at follow-up compared with all other clusters. Similarly, an interaction was observed between DT and A/D that predicted risk for AN.DiscussionHaving elevated DT and A/D scores may increase risk for eating disorder symptomatology above and beyond a high score on either alone. Findings suggest that cluster modeling based on DT and A/D may be useful to inform novel and useful intervention strategies for AN and BN in adolescents. © 2015 Wiley Periodicals, Inc. (Int J Eat Disord 2015)
    International Journal of Eating Disorders 05/2015; DOI:10.1002/eat.22431 · 3.03 Impact Factor
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    ABSTRACT: We examined how genotype-environment correlation processes differ as a function of adolescent age. We tested whether adolescent age moderates genetic and environmental influences on positivity and negativity in mother-adolescent and father-adolescent relationships using parallel samples of twin parents from the Twin and Offspring Study in Sweden and twin/sibling adolescents from the Nonshared Environment in Adolescent Development Study. We inferred differences in the role of passive and nonpassive genotype-environment correlation based on biometric moderation findings. The findings indicated that nonpassive gene-environment correlation played a stronger role for positivity in mother- and father-adolescent relationships in families with older adolescents than in families with younger adolescents, and that passive gene-environment correlation played a stronger role for positivity in the mother-adolescent relationship in families with younger adolescents than in families with older adolescents. Implications of these findings for the timing and targeting of interventions on family relationships are discussed.
    Development and Psychopathology 04/2015; DOI:10.1017/S0954579415000358 · 4.89 Impact Factor
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    ABSTRACT: Prior twin and adoption studies have demonstrated the importance of both genetic and shared environmental factors in the etiology of criminal behavior (CB). However, despite substantial interest in life-course theories of CB, few genetically informative studies have examined CB in a developmental context. In 69,767 male-male twin pairs and full-sibling pairs with ≤ 2 years' difference in age, born 1958-1976 and ascertained from the Swedish Twin and Population Registries, we obtained information on all criminal convictions from 1973 to 2011 from the Swedish Crime Register. We fitted a Cholesky structural model, using the OpenMx package, to CB in these pairs over three age periods: 15-19, 20-24, and 25-29. The Cholesky model had two main genetic factors. The first began at ages 15-19 and declined in importance over development. The second started at ages 20-24 and was stable over time. Only one major shared environmental factor was seen, beginning at ages 15-19. Heritability for CB declined from ages 15-29, as did shared environmental effects, although at a slower rate. Genetic risk factors for CB in males are developmentally dynamic, demonstrating both innovation and attenuation. These results are consistent with theories of adolescent-limited and life-course persistent CB subtypes. Heritability for CB did not increase over time as might be predicted from active gene-environmental correlation. However, consistent with expectation, the proportion of variability explained by shared environmental effects declined slightly as individuals aged and moved away from their original homes and neighborhoods.
    Twin Research and Human Genetics 04/2015; 18(03):1-7. DOI:10.1017/thg.2015.25 · 1.92 Impact Factor
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    ABSTRACT: To compare the annual prevalence of the autism symptom phenotype and of registered diagnoses for autism spectrum disorder during a 10 year period in children. Population based study. Child and Adolescent Twin Study and national patient register, Sweden. 19 993 twins (190 with autism spectrum disorder) and all children (n=1 078 975; 4620 with autism spectrum disorder) born in Sweden over a 10 year period from 1993 to 2002. Annual prevalence of the autism symptom phenotype (that is, symptoms on which the diagnostic criteria are based) assessed by a validated parental telephone interview (the Autism-Tics, ADHD and other Comorbidities inventory), and annual prevalence of reported diagnoses of autism spectrum disorder in the national patient register. The annual prevalence of the autism symptom phenotype was stable during the 10 year period (P=0.87 for linear time trend). In contrast, there was a monotonic significant increase in prevalence of registered diagnoses of autism spectrum disorder in the national patient register (P<0.001 for linear trend). The prevalence of the autism symptom phenotype has remained stable in children in Sweden while the official prevalence for registered, clinically diagnosed, autism spectrum disorder has increased substantially. This suggests that administrative changes, affecting the registered prevalence, rather than secular factors affecting the pathogenesis, are important for the increase in reported prevalence of autism spectrum disorder. © Lundström et al 2015.
    BMJ (online) 04/2015; 350(apr28 2):h1961. DOI:10.1136/bmj.h1961 · 16.38 Impact Factor
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    ABSTRACT: Little is known about genetic influences on juvenile irritability and whether such influences are developmentally stable and/or dynamic. This study examined the temporal pattern of genetic and environmental effects on irritability using data from a prospective, four-wave longitudinal twin study. Parents and their twin children (N=2,620 children) from the Swedish Twin Study of Child and Adolescent Development reported on the children's irritability, defined using a previously identified scale from the Child Behavior Checklist. Genetic effects differed across the sexes, with males exhibiting increasing heritability from early childhood through young adulthood and females exhibiting decreasing heritability. Genetic innovation was also more prominent in males than in females, with new genetic risk factors affecting irritability in early and late adolescence for males. Shared environment was not a primary influence on irritability for males or females. Unique, nonshared environmental factors suggested strong effects early for males followed by an attenuating influence, whereas unique environmental factors were relatively stable for females. Genetic effects on irritability are developmentally dynamic from middle childhood through young adulthood, with males and females displaying differing patterns. As males age, genetic influences on irritability increase while nonshared environmental influences weaken. Genetic contributions are quite strong in females early in life but decline in importance with age. In girls, nonshared environmental influences are fairly stable throughout development.
    American Journal of Psychiatry 04/2015; DOI:10.1176/appi.ajp.2015.14040509 · 13.56 Impact Factor
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    ABSTRACT: The transmission of anxiety within families is well recognized, but the underlying processes are poorly understood. Twin studies of adolescent anxiety demonstrate both genetic and environmental influence, and multiple aspects of parenting are associated with offspring anxiety. To date, the children-of-twins design has not been used to evaluate the relative contributions of genetic transmission compared with direct transmission of anxiety from parents to their offspring. Anxiety and neuroticism measures were completed by 385 monozygotic and 486 dizygotic same-sex twin families (37% male twin pair families) from the Twin and Offspring Study in Sweden. Structural equation models tested for the presence of both genetic and environmental transmission from one generation to the next. For both anxiety and neuroticism, the models provide support for significant direct environmental transmission from parents to their adolescent offspring. In contrast, there was no evidence of significant genetic transmission. The association between parental and offspring anxiety largely arises because of a direct association between parents and their children independent of genetic confounds. The lack of genetic transmission may reflect there being different genetic effects on these traits in adolescence and adulthood. Direct environmental transmission is in line with developmental theories of anxiety suggesting that children and adolescents learn anxious behaviors from their parents through a number of pathways such as modeling. Future analyses should combine children-of-twins data with child twin data in order to examine whether this direct effect solely represents parental influences on the offspring or whether it also includes child/adolescent anxiety evoking parental anxiety.
    American Journal of Psychiatry 04/2015; DOI:10.1176/appi.ajp.2015.14070818 · 13.56 Impact Factor
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    ABSTRACT: Asthma is a common childhood disease and several risk factors have been identified; however, the impact of genes and environment is not fully understood. The aim of the Swedish Twin study On Prediction and Prevention of Asthma (STOPPA) is to identify environmental (birth characteristics and early life) and genetic (including epigenetic) factors as determinants for asthmatic disease. Based on the Child and Adolescent Twin Study in Sweden (CATSS) (parental interview at 9 or 12 years, N ~23,900) and an asthma and/or wheezing algorithm, we identified a sample of monozygotic (MZ) and dizygotic (DZ) same-sexed twin pairs. The twin pairs were classified as asthma concordant (ACC), asthma discordant (ADC) and healthy concordant (HCC). A sample of 9- to 14-year-old twins and their parents were invited to participate in a clinical examination. Background characteristics were collected in questionnaires and obtained from the National Health Registers. A clinical examination was performed to test lung function and capacity (spirometry with reversibility test and exhaled nitric oxide) and collect blood (serology and DNA), urine (metabolites), feces (microbiota), and saliva (cortisol). In total, 376 twin pairs (752 individual twins) completed the study, response rate 52%. All participating twins answered the questionnaire and >90% participated in lung function testing, blood-, and saliva sampling. This article describes the design, recruitment, data collection, measures, and background characteristics, as well as ongoing and planned analyses in STOPPA. Potential gains of the study include the identification of biomarkers, the emergence of candidates for drug development, and new leads for prevention of asthma and allergic disease.
    Twin Research and Human Genetics 04/2015; 18(03):1-8. DOI:10.1017/thg.2015.17 · 1.92 Impact Factor
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    ABSTRACT: Background: Sexual crime is an important public health concern. The possible causes of sexual aggression, however, remain insufficiently known. Methods: We examined familial aggregation and the contribution of genetic and environmental factors to sexual crime by linking longitudinal, nationwide Swedish crime and multigenerational family registers. We included all men convicted of any sexual offence (N=21,566), specifically rape of an adult (N=6,131), and child molestation (N=4,465), from 1973 to 2009. Sexual crime rates among fathers and brothers of sexual offenders were compared with corresponding rates in fathers and brothers of age-matched population control men without sexual crime convictions. We also modelled the relative influence of genetic and environmental factors to the liability of sexual offending. Results: We found strong familial aggregation of sexual crime (odds ratio [OR]=5.1; 95% CI=4.5-5.9) among full brothers of convicted sexual offenders. Familial aggregation was lower in father-son dyads (OR=3.7, 95% CI=3.2-4.4) and among half-brothers (OR=2.1, 95% CI=1.5-19.8). Statistical modelling of the strength and patterns of familial aggregation suggested that genetic factors (40%) and non-shared environmental factors, including measurement error (58%) explained the liability to offend sexually better than shared environmental influences (2%). Further, genetic effects tended to be weaker for rape of an adult (19%) than for child molestation (46%). Conclusions: We report strong evidence of familial clustering of sexual offending, primarily accounted for by genes rather than shared environmental influences. Future research should possibly test the effectiveness of selective prevention efforts for male first-degree relatives of sexually aggressive individuals, and consider familial risk in sexual violence risk assessment.
    International Journal of Epidemiology 04/2015; in press. DOI:10.1093/ije/dyv029 · 9.20 Impact Factor

Publication Stats

17k Citations
3,180.04 Total Impact Points

Institutions

  • 2009–2015
    • University of Oxford
      • Department of Psychiatry
      Oxford, England, United Kingdom
    • Virginia Commonwealth University
      • Department of Psychology
      Richmond, VA, United States
  • 1994–2015
    • Karolinska Institutet
      • • Department of Medical Epidemiology and Biostatistics
      • • Institutet för miljömedicin - IMM
      Solna, Stockholm, Sweden
  • 2014
    • City of Stockholm
      Tukholma, Stockholm, Sweden
  • 2010–2014
    • Indiana University Bloomington
      • Department of Psychological and Brain Sciences
      Bloomington, Indiana, United States
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2005–2014
    • University of Gothenburg
      • • Institute of Neuroscience and Physiology
      • • Department of Psychology
      Goeteborg, Västra Götaland, Sweden
  • 2001–2014
    • Karolinska University Hospital
      Tukholma, Stockholm, Sweden
  • 2013
    • Indiana University Health
      Bloomington, Indiana, United States
  • 2005–2013
    • University of Southern California
      • Department of Psychology
      Los Ángeles, California, United States
  • 2009–2012
    • Lund University
      • • Department of Clinical Sciences, Malmö
      • • School of Social Work
      Lund, Skåne, Sweden
  • 2006–2012
    • University of North Carolina at Chapel Hill
      • Department of Psychiatry
      North Carolina, United States
  • 2008–2009
    • Stockholm School of Economics
      • Department of Economics
      Stockholm, Stockholm, Sweden
    • George Washington University
      • Department of Psychology
      Washington, D. C., DC, United States
  • 2000–2007
    • Uppsala University
      • Department of Women's and Children's Health
      Uppsala, Uppsala, Sweden
  • 2004
    • Stockholm University
      Tukholma, Stockholm, Sweden
  • 2003
    • Max Planck Institute for Demographic Research
      Rostock, Mecklenburg-Vorpommern, Germany
  • 1999
    • University of Helsinki
      • Department of Medical Genetics
      Helsinki, Province of Southern Finland, Finland
  • 1993
    • Pennsylvania State University
      University Park, Maryland, United States