Paul Lichtenstein

Karolinska Institutet, Solna, Stockholm, Sweden

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Publications (397)2658.55 Total impact

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    ABSTRACT: We aimed to provide unbiased estimates of familial risk and heritability of social anxiety disorder (SAD) and avoidant personality disorder (AVPD).
    Psychological medicine. 09/2014;
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    ABSTRACT: Objectives Darier disease is an autosomal dominant skin disorder caused by mutations in the ATPase, Ca++ transporting, cardiac muscle, slow twitch 2 (ATP2A2) gene and previously reported to cosegregate with bipolar disorder and schizophrenia in occasional pedigrees. It is, however, unknown whether these associations exist also in the general population, and the objective of this study was to examine this question. Methods We compared a national sample of individuals with Darier disease and their first-degree relatives with matched unexposed individuals from the general population and their first-degree relatives, respectively. To examine risks for bipolar disorder and schizophrenia, risk ratios and 95% confidence intervals (CIs) were estimated using conditional logistic regressions. Results Individuals with Darier disease had a 4.3 times higher risk of being diagnosed with bipolar disorder (95% CI: 2.6–7.3) and a 2.3 times higher risk of being diagnosed with schizophrenia (95% CI: 1.1–5.2) than matched individuals from the general population. Relatives of individuals with Darier disease had a 1.6 times higher risk of having bipolar disorder (95% CI: 1.1–2.5) than relatives of matched individuals from the general population, but no increased risk of schizophrenia (risk ratio = 0.8, 95% CI: 0.4–1.8). Conclusions The association between Darier disease and bipolar disorder is manifest also in the population, and our data suggest that genetic variability within the ATP2A2 gene that causes Darier disease also confers susceptibility for bipolar disorder. The Darier-causing mutations merit additional attention in molecular genetic research on bipolar disorder.
    Bipolar Disorders 09/2014; · 4.62 Impact Factor
  • Brian M D'Onofrio, Arvid Sjölander, Paul Lichtenstein
    JAMA Psychiatry 09/2014; 71(9):1078-1079. · 12.01 Impact Factor
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    ABSTRACT: Background There are persistent concerns of long-term effects of stimulant ADHD medication on the development of substance abuse.Methods Using Swedish national registers, we studied all individuals born between 1960 and 1998 and diagnosed with ADHD (26,249 men and 12,504 women). We investigated the association between stimulant ADHD medication in 2006 and substance abuse during 2009. Substance abuse was indexed by substance-related death, crime, or hospital visits.ResultsADHD medication was not associated with increased rate of substance abuse. Actually, the rate during 2009 was 31% lower among those prescribed ADHD medication in 2006, even after controlling for medication in 2009 and other covariates (hazard ratio: 0.69; 95% confidence interval: 0.57–0.84). Also, the longer the duration of medication, the lower the rate of substance abuse. Similar risk reductions were suggested among children and when investigating the association between stimulant ADHD medication and concomitant short-term abuse.Conclusions We found no indication of increased risks of substance abuse among individuals prescribed stimulant ADHD medication; if anything, the data suggested a long-term protective effect on substance abuse. Although stimulant ADHD medication does not seem to increase the risk for substance abuse, clinicians should remain alert to the potential problem of stimulant misuse and diversion in ADHD patients.
    Journal of Child Psychology and Psychiatry 08/2014; 55(8). · 5.42 Impact Factor
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    ABSTRACT: Objectives Bipolar disorder (BPD) shares genetic components with other psychiatric disorders; however, uncertainty remains about where in the psychiatric spectra BPD falls. To understand the etiology of BPD, we studied the familial aggregation of BPD and co-aggregation between BPD and schizophrenia, depression, anxiety disorders, attention-deficit hyperactivity disorder, drug abuse, personality disorders, and autism spectrum disorders.MethodsA population-based cohort was created by linking several Swedish national registers. A total of 54,723 individuals with BPD were identified among 8,141,033 offspring from 4,149,748 nuclear families. The relative risk of BPD in relatives and the co-occurrence of other psychiatric disorders in patients with BPD and their relatives were compared to those of matched-population controls. Structural equation modeling was used to estimate the heritability and tetrachoric correlation.ResultsThe familial risks for relatives of BPD probands were 5.8–7.9 in first-degree relatives, and decreased with genetic distance. Co-occurrence risks for other psychiatric disorders were 9.7–22.9 in individuals with BPD and 1.7–2.8 in full siblings of BPD probands. Heritability for BPD was estimated at 58%. The correlations between BPD and other psychiatric disorders were considerable (0.37–0.62) and primarily due to genetic effects. The correlation with depression was the highest (0.62), and was 0.44 for schizophrenia.Conclusions The high familial risks provide evidence that genetic factors play an important role in the etiology of BPD, and the shared genetic determinants suggest pleiotropic effects across different psychiatric disorders. Results also indicate that BPD is in both the mood and psychotic spectra, but possibly more closely related to mood disorders.
    Bipolar Disorders 08/2014; · 4.62 Impact Factor
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    ABSTRACT: To compare risks for suicidality and criminality in a national cohort of people diagnosed with bipolar disorder, and to assess how risk factor profiles differ between these outcomes.
    The Journal of clinical psychiatry. 08/2014; 75(8):e809-16.
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    ABSTRACT: Introduction: The study of differences between monozygotic (MZ) twin pairs with respect to ADHD may provide novel leads to disentangle the environmental contribution driving its phenotypes. Objectives: To examine non-shared environmental influences on executive function in dimensionally defined ADHD. Methods: This study included 27 MZ twin pairs (7 female) aged 11–20 years being moderately to substantially discordant for ADHD traits as assessed by the Attention Problem (AP) scale of the Child Behavior Checklist/Adult Behavior Checklist. The twins completed the Wisconsin Card Sorting Test (WCST) for cognitive flexibility and the Tower Test (TT) for foresighted planning. Two statistical approaches were used to analyze the data. First, correlations between ADHD trait intra-pair differences and WCST and TT scores were calculated. Second, the significance of those intra-pair differences on WCST and TT, using ADHD as categorical variable in clinically discordant pairs, was tested. Results: Both analysing strategies revealed a link between ADHD on one hand, and foresighted planning and inhibitory control on the other hand mediated by non-shared environmental factors. The first statistical approach yielded positive correlations between intra-pairs differences on the AP scale and intra-pair differences on two subscales of the TT: total rule violation (r s 50 . 41) and rule-violation-per-item-ratio (r s 50 . 38). Findings in categorically discordant pairs were consistent, showing within-pair differences on the same subtests (z-1 . 63, P50 . 05, one-tailed and z521 . 60, P50 . 05, one-tailed). Conclusions: Findings confirm previous research suggesting ADHD to be a quantitative extreme on a continuum with executive functions being a cognitive marker of ADHD traits. Non-shared environmental factors appear to influence planning skills and inhibitory control. Introduction Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by motor overactivity, inattention and impulsivity. The defining criteria for ADHD outlined by the recently published 5th edition of the Diagnostic and Statistical Manual (DSM-5; American Psychiatric Association, 2013) include international journal of developmental
    07/2014;
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    ABSTRACT: Hypospadias (aberrant opening of the urethra on the underside of the penis) occurs in 1 per 300 newborn boys. It has been previously unknown whether this common malformation is associated with increased psychiatric morbidity later in life. Studies of individuals with hypospadias also provide an opportunity to examine whether difference in androgen signaling is related to neurodevelopmental disorders. To elucidate the mechanisms behind a possible association, we also studied psychiatric outcomes among brothers of the hypospadias patients.
    Journal of Child Psychology and Psychiatry 07/2014; · 5.42 Impact Factor
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    ABSTRACT: The etiology of major depressive disorder (MDD) is likely to be heterogeneous, but postpartum depression (PPD) is hypothesized to represent a more homogenous subset of MDD. We use genome-wide SNP data to explore this hypothesis. We assembled a total cohort of 1,420 self-report cases of PPD and 9,473 controls with genome-wide genotypes from Australia, The Netherlands, Sweden and the UK. We estimated the total variance attributable to genotyped variants. We used association results from the Psychiatric Genomics Consortia (PGC) of bipolar disorder (BPD) and MDD to create polygenic scores in PPD and related MDD data sets to estimate the genetic overlap between the disorders. We estimated that the percentage of variance on the liability scale explained by common genetic variants to be 0.22 with a standard error of 0.12, p = 0.02. The proportion of variance (R (2)) from a logistic regression of PPD case/control status in all four cohorts on a SNP profile score weighted by PGC-BPD association results was small (0.1 %) but significant (p = 0.004) indicating a genetic overlap between BPD and PPD. The results were highly significant in the Australian and Dutch cohorts (R (2) > 1.1 %, p < 0.008), where the majority of cases met criteria for MDD. The genetic overlap between BPD and MDD was not significant in larger Australian and Dutch MDD case/control cohorts after excluding PPD cases (R (2) = 0.06 %, p = 0.08), despite the larger MDD group affording more power. Our results suggest an empirical genetic evidence for a more important shared genetic etiology between BPD and PPD than between BPD and MDD.
    Archives of Women s Mental Health 07/2014; · 2.01 Impact Factor
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    ABSTRACT: Psychiatric disorders are known to be prevalent in multiple sclerosis (MS).OBJECTIVE: The objective of this paper is to study comorbidity between MS and bipolar disorder, schizophrenia and depression in a nationwide cohort and to determine whether shared genetic liability underlies the putative association.METHODS: We identified ICD-diagnosed patients with MS (n = 16,467), bipolar disorder (n = 30,761), schizophrenia (n = 22,781) and depression (n = 172,479) in the Swedish National Patient Register and identified their siblings in the Multi-Generation Register. The risk of MS was compared in psychiatric patients and in matched unexposed individuals. Shared familial risk between MS and psychiatric disorders was estimated by sibling comparison.RESULTS: The risk of MS was increased in patients with bipolar disorder (hazard ratio (HR) 1.8, 95% confidence interval (CI) 1.6-2.2, p < 0.0001) and depression (HR 1.9, 95% CI 1.7-2.0, p < 0.0001). MS risk in schizophrenia was decreased (HR 0.6, 95% CI 0.4-0.9, p = 0.005). The association between having a sibling with a psychiatric disorder and developing MS was not significant.CONCLUSION: We found a strong positive association between MS and bipolar disorder and depression that could not be explained by genetic liability. The unexpected negative association between MS and schizophrenia might be spurious or indicate possible protective mechanisms that warrant further exploration.
    Multiple sclerosis (Houndmills, Basingstoke, England). 07/2014;
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    ABSTRACT: Background Studies have found an association between low birth weight and ADHD, but the nature of this relation is unclear. First, it is uncertain whether birth weight is associated with both of the ADHD dimensions, inattentiveness and hyperactivity-impulsivity. Second, it remains uncertain whether the association between birth weight and ADHD symptom severity is confounded by familial factors.Method Parents of all Swedish 9- and 12-year-old twins born between 1992 and 2000 were interviewed for DSM-IV inattentive and hyperactive-impulsive ADHD symptoms by the Autism – Tics, AD/HD and other Comorbidities (A-TAC) inventory (N = 21,775 twins). Birth weight was collected prospectively through the Medical Birth Registry. We used a within-twin pair design to control for genetic and shared environmental factors.ResultsReduced birth weight was significantly associated with a mean increase in total ADHD (β = −.42; 95% CI: −.53, −.30), inattentive (β = −.26; 95% CI: −.33, −.19), and hyperactive-impulsive (β = −.16; 95% CI: −.22, −.10) symptom severity. These results imply that a change of one kilogram of birth weight corresponded to parents rating their child nearly one unit higher (going from “no” to “yes, to some extent” on a given symptom) on the total ADHD scale. These associations remained within pairs of MZ and DZ twins, and were also present when restricting the analyses to full term births.Conclusions There is an independent association between low birth weight and all forms of ADHD symptoms, even after controlling for all environmental and genetic confounds shared within twin pairs. These results indicate that fetal growth restriction (as reflected in birth weight differences within twin pairs) and/or the environmental factors which influence it is in the casual pathway leading to ADHD.
    Journal of Child Psychology and Psychiatry 07/2014; · 5.42 Impact Factor
  • Seena Fazel, Paul Lichtenstein, Niklas Långström
    JAMA Psychiatry 07/2014; 71(7):840. · 12.01 Impact Factor
  • Therese Ljung, Qi Chen, Paul Lichtenstein, Henrik Larsson
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    ABSTRACT: The prevention of suicidal behavior is one of the most important tasks for mental health clinicians. Although a few studies have indicated an increased risk of suicidal behavior among individuals with attention-deficit/hyperactivity disorder, the development of more effective ways of identifying and modifying the risk is hampered by our limited understanding of the underlying mechanisms for this association.
    JAMA Psychiatry 06/2014; · 12.01 Impact Factor
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    ABSTRACT: OBJECTIVE This study examined the risk of antidepressant-induced manic switch in patients with bipolar disorder treated either with antidepressant monotherapy or with an antidepressant in conjunction with a mood stabilizer. METHOD Using Swedish national registries, the authors identified 3,240 patients with bipolar disorder who started treatment with an antidepressant and had no antidepressant treatment during the previous year. Patients were categorized into those receiving antidepressant monotherapy and those receiving an antidepressant plus a mood stabilizer. A within-individual design was used to control for confounding by disorder severity, genetic makeup, and early environmental factors. Cox regression analyses conditioned on individual were used to compare the rate of mania 0-3 months and 3-9 months after the start of antidepressant treatment with a preceding non-treatment period. RESULTS Nearly 35% of the patients were treated with antidepressant monotherapy. The increased risk of treatment-emergent mania was confined to patients on antidepressant monotherapy (hazard ratio=2.83, 95% CI=1.12, 7.19). Among patients treated with a concurrent mood stabilizer, no acute change in risk of mania was observed during the 3 months after the start of antidepressant treatment (hazard ratio=0.79, 95% CI=0.54, 1.15), and a decreased risk was observed during the period 3-9 months after treatment initiation (hazard ratio=0.63, 95% CI=0.42, 0.93). CONCLUSIONS In this national registry study, antidepressant monotherapy was associated with an increased risk of mania. However, no risk of mania was seen in patients receiving an antidepressant while treated with a mood stabilizer. The results highlight the importance of avoiding antidepressant monotherapy in the treatment of bipolar disorder.
    American Journal of Psychiatry 06/2014; · 14.72 Impact Factor
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    ABSTRACT: Background: Low socioeconomic status in childhood is a well-known predictor of subsequent criminal and substance misuse behaviors but the causal mechanisms are questioned. Aims: To investigate whether childhood family income predicts subsequent violent criminality and substance misuse and whether the associations are in turn explained by unobserved familial risk factors. Method: Nationwide Swedish quasi-experimental, family-based study following cohorts born 1989-1993 (n_total=526,167; n_cousins=262,267; n_siblings=216,424) between ages 15-21 years. Results: Children of parents in the lowest income quintile experienced a seven-fold increased hazard rate of being convicted of violent criminality compared to peers in the highest quintile (HR=6.84, 95% CI: 6.28-7.44). This association was entirely accounted for by unobserved familial risk factors (HR=0.99; 95% CI: 0.46-2.13). Similar pattern of effects was found for substance misuse. Conclusions: There are no associations between childhood family income and subsequent violent criminality and substance misuse once unobserved familial risk factors are adjusted for.
    The British Journal of Psychiatry 06/2014; In press. · 6.61 Impact Factor
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    ABSTRACT: People living in densely populated and socially disorganized areas have higher rates of psychiatric morbidity but the potential causal status of such factors is uncertain. We used nationwide Swedish longitudinal registry data to identify all children born 1967-1989 (n=2,361,585), including separate datasets for all cousins (n=1,715,059) and siblings (n=1,667,894). The nature of the associations between population density and neighborhood deprivation and individual risk for a schizophrenia diagnosis were investigated while adjusting for unobserved familial risk factors (through cousin and sibling-comparisons), and then compared with similar associations for depression. We generated familial pedigree structures using the Multi-Generation Registry and identified study participants with schizophrenia and depression using the National Patient Registry. Fixed-effects logistic regression models were used to study within-family estimates. Population density, measured as ln(population size/km^2), at age 15 predicted subsequent schizophrenia in the population (OR=1.10; 95% CI 1.09-1.11). Unobserved familial risk factors shared by cousins within extended families attenuated the association (1.06; 1.03-1.10) and the link disappeared entirely within nuclear families (1.02; 0.97-1.08). Similar results were found for neighborhood deprivation as predictor and for depression as outcome. Sensitivity tests demonstrated that timing and accumulation effects of the exposures (mean scores across birth, ages 1-5, 6-10 and 11- 15 years) did not alter the findings. Excess risks of psychiatric morbidity, particularly schizophrenia, in densely populated and socioeconomically deprived Swedish neighborhoods appear therefore to result primarily from unobserved familial selection factors. Previous studies may have overemphasized the etiological importance of these environmental factors.
    Schizophrenia Bulletin 06/2014; Advance Access. · 8.80 Impact Factor
  • The British Journal of Psychiatry 06/2014; In press. · 6.61 Impact Factor
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    Seena Fazel, Achim Wolf, Camilla Palm, Paul Lichtenstein
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    ABSTRACT: Background People with schizophrenia and related disorders are at an increased risk of adverse outcomes, including conviction of a violent offence, suicide, and premature mortality. However, the rates of, and risk factors for, these outcomes need clarification as a basis for population-based and targeted interventions. We aimed to determine rates and risk factors for these outcomes, and investigate to what extent they are shared across outcomes and are specific to schizophrenia and related disorders. Methods We undertook a total population cohort study in Sweden of 24 297 patients with schizophrenia and related disorders between January, 1972 and December, 2009. Patients were matched by age and sex to people from the general population (n=485 940) and also to unaffected sibling controls (n=26 357). First, we investigated rates of conviction of a violent offence, suicide, and premature mortality, with follow-up until conviction of a violent offence, emigration, death, or end of follow-up (Dec 31, 2009), whichever occurred first. Second, we analysed associations between these adverse outcomes and sociodemographic, individual, familial, and distal risk factors, for men and women separately, with Cox proportional hazards models. Finally, we assessed time trends in adverse outcomes between 1972 and 2009, for which we compared patients with unaffected siblings, and analysed associations with changes in the number of nights spent in inpatient beds in psychiatric facilities nationwide. Findings Within 5 years of their initial diagnosis, 13·9% of men and 4·7% of women with schizophrenia and related disorders had a major adverse outcome (10·7% of men and 2·7% of women were convicted of a violent offence, and 3·3% of men and 2·0% of women died prematurely of any cause). During the study, the adjusted odds ratio of any adverse outcomes for patients compared with general population controls was 7·5 (95% CI 7·2–7·9) in men and 11·1 (10·2–12·1) in women. Three risk factors that were present before diagnosis were predictive of any adverse outcome: drug use disorders, criminality, and self-harm, which were also risk factors for these outcomes in unaffected siblings and in the general population. Over the period 1973–2009, the odds of these outcomes increased in patients with schizophrenia and related disorders compared with unaffected siblings. Interpretation Schizophrenia and related disorders are associated with substantially increased rates of violent crime, suicide, and premature mortality. Risk factors for these three outcomes included both those specific to individuals with schizophrenia and related disorders, and those shared with the general population. Therefore, a combination of population-based and targeted strategies might be necessary to reduce the substantial rates of adverse outcomes in patients with schizophrenia and related disorders. Funding Wellcome Trust and The Swedish Research Council.
    The Lancet Psychiatry 06/2014; 1(1):44-54.
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    Ian Kelleher, Martin Cederlöf, Paul Lichtenstein
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    ABSTRACT: Psychotic experiences are far more prevalent in the population than psychotic disorders and are associated with a wide range of depressive, anxiety and behavioral disorders, as well as increased risk for psychotic disorder. Recently, psychotic experiences have been highlighted as a potentially valuable clinical marker of risk for suicidal behavior. There have been few studies to date, however, to assess psychotic experiences as a predictor of suicidality over time. We wished to assess whether young persons with suicidal ideation at baseline assessment who reported psychotic experiences were at higher risk for persistence of suicidal ideation at follow-up than young persons who also reported suicidal ideation at baseline but who did not report co-occurring psychotic experiences. A total of 2,263 adolescents were assessed at age 13 to 14 years for psychotic experiences, suicidal ideation and internalizing and externalizing psychopathology. Participants were re-assessed at ages 16 to 17 years and 19 to 20 years. Among 13- to 14-year olds with suicidal ideation, co-occurring psychotic experiences did not predict an increased odds of persistence of suicidal ideation to age 16 to 17 years (OR=0.94, 95% CI: 0.19-4.78). Among 16- to 17-year olds with suicidal ideation, however, co-occurring psychotic experiences predicted a 6-fold increased odds of persistence of suicidal ideation to age 19 to 20 years (OR=5.53, 95% CI: 1.33-23.00). Psychotic experiences are an important but under-recognized marker of risk for persistence of suicidal ideation, in particular from mid-adolescence. An increased emphasis on the clinical assessment of psychotic experiences in mental health services should be a priority.
    World psychiatry: official journal of the World Psychiatric Association (WPA) 06/2014; 13(2):184-8. · 8.97 Impact Factor
  • S. Kyaga, P. Lichtenstein, M. Boman, M. Landén
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    ABSTRACT: Objective To investigate whether persons with bipolar disorder and their siblings have leadership traits and are overrepresented in executive professions.MethodA nested case-control study based on longitudinal Swedish total population registries. Data from officer suitability interviews (n = 1 126 519), and information on occupations were collected. Bipolar patients (n = 68 915) and their healthy siblings were compared with controls.ResultsBipolar patients without comorbidity (pure; n = 22 980) were overrepresented in both the highest and lowest strata of officer suitability; their healthy siblings in the highest strata only. Patients with pure bipolar disorder were underrepresented in executive professions, whereas their siblings were overrepresented in these professions (particularly political professions). Patients with general bipolar disorder (including those with comorbidities) and their healthy siblings were overrepresented only in the lowest strata of officer suitability ratings. General bipolar patients were underrepresented in executive professions, whereas their siblings had similar rates of executive professions as controls. Adjusting results for IQ slightly attenuated point estimates, but resulted in pure bipolar patients and their siblings no longer being significantly overrepresented in superior strata of officer suitability, and siblings no longer being overrepresented in executive professions.Conclusion Results support that traits associated with bipolar disorder are linked to superior leadership qualities.
    Acta Psychiatrica Scandinavica 06/2014; · 4.86 Impact Factor

Publication Stats

12k Citations
2,658.55 Total Impact Points

Institutions

  • 1993–2014
    • Karolinska Institutet
      • • Department of Medical Epidemiology and Biostatistics
      • • Institutet för miljömedicin - IMM
      Solna, Stockholm, Sweden
  • 2013
    • Indiana University East
      Indiana, United States
    • Maastricht University
      Maestricht, Limburg, Netherlands
  • 2010–2013
    • Indiana University Bloomington
      • Department of Psychological and Brain Sciences
      Bloomington, IN, United States
    • Johns Hopkins University
      Baltimore, Maryland, United States
    • Harvard Medical School
      Boston, Massachusetts, United States
  • 2008–2013
    • University of Gothenburg
      • Institute of Neuroscience and Physiology
      Goeteborg, Västra Götaland, Sweden
    • Virginia Commonwealth University
      • • Department of Psychiatry
      • • Virginia Institute for Psychiatric and Behavioral Genetics
      • • Department of Psychology
      Richmond, VA, United States
    • Stockholm School of Economics
      • Department of Economics
      Stockholm, Stockholm, Sweden
    • Uppsala University Hospital
      • Department of Neuroscience
      Uppsala, Uppsala, Sweden
  • 2006–2013
    • University of North Carolina at Chapel Hill
      • • Department of Psychiatry
      • • Department of Genetics
      Chapel Hill, NC, United States
  • 2000–2013
    • University of Oxford
      • • Department of Psychiatry
      • • Cancer Epidemiology Unit
      Oxford, ENG, United Kingdom
    • Uppsala University
      • Department of Mathematics
      Uppsala, Uppsala, Sweden
  • 2012
    • Cornell University
      Ithaca, New York, United States
    • Massachusetts General Hospital
      • Psychiatric and Neurodevelopment Genetics Unit
      Boston, MA, United States
  • 2010–2012
    • Pennsylvania State University
      • Department of Psychology
      State College, PA, United States
  • 2008–2012
    • Lund University
      • Department of Clinical Sciences
      Lund, Skane, Sweden
  • 2011
    • Örebro University Hospital
      Örebro, Örebro, Sweden
    • Northwestern University
      • Roxelyn and Richard Pepper Department of Communication Sciences and Disorders
      Evanston, IL, United States
    • University of Bristol
      • MRC Centre for Causal Analyses in Translational Epidemiology
      Bristol, ENG, United Kingdom
    • Cardiff University
      • Department of Psychological Medicine and Neurology
      Cardiff, WLS, United Kingdom
    • National University of Singapore
      • Saw Swee Hock School of Public Health
      Singapore, Singapore
    • The University of Manchester
      Manchester, England, United Kingdom
    • Birkbeck, University of London
      • Department of Psychological Sciences
      London, ENG, United Kingdom
    • Linköping University
      • Department of Clinical and Experimental Medicine (IKE)
      Sweden
  • 2005–2011
    • University of Southern California
      • Department of Psychology
      Los Angeles, CA, United States
    • Simon Fraser University
      • Faculty of Health Sciences
      Burnaby, British Columbia, Canada
  • 2008–2009
    • Massachusetts Institute of Technology
      • Department of Economics
      Cambridge, MA, United States
    • George Washington University
      • Department of Psychology
      Washington, Washington, D.C., United States
  • 2004–2008
    • Karolinska University Hospital
      Tukholma, Stockholm, Sweden
    • Università commerciale Luigi Bocconi
      Milano, Lombardy, Italy
  • 2007
    • King's College London
      • Institute of Psychiatry
      London, ENG, United Kingdom
    • University Hospital of Lausanne
      • Institut universitaire de médecine sociale et préventive
      Lausanne, VD, Switzerland
  • 2002–2004
    • Max Planck Institute for Demographic Research
      Rostock, Mecklenburg-Vorpommern, Germany
  • 1999
    • University of Helsinki
      • Department of Medical Genetics
      Helsinki, Province of Southern Finland, Finland