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  • 1.
    Baker, J. H.
    et al.
    Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond, USA; Department of Psychology, Virginia Commonwealth University, Richmond, USA.
    Maes, H. H.
    Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond, USA; Department of Human Genetics, Virginia Commonwealth University, Richmond, USA; Massey Cancer Center, Virginia Commonwealth University, Richmond, USA.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kendler, K. S.
    Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond, USA; Department of Human Genetics, Virginia Commonwealth University, Richmond, USA; Department of Psychiatry, Virginia Commonwealth University, Richmond, USA.
    Sex differences and developmental stability in genetic and environmental influences on psychoactive substance consumption from early adolescence to young adulthood2011In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 41, no 9, p. 1907-1916Article in journal (Refereed)
    Abstract [en]

    Background: Genetic and environmental factors are important in the etiology of substance use. However, little is known about the stability of these factors across development. We aimed to answer three crucial questions about this etiology that have never been addressed in a single study: (1) Is there a general vulnerability to substance consumption from early adolescence to young adulthood? (2) If so, do the genetic and environmental influences on this vulnerability change across development? (3) Do these developmental processes differ in males and females?

    Method: Subjects included 1480 twin pairs from the Swedish Twin Study of Child and Adolescent Development who have been followed since 1994. Prospective, self-reported regular smoking, alcohol intoxication and illicit drug use were assessed at ages 13-14, 16-17 and 19-20 years. Structural modeling was performed with the program Mx.

    Results: An underlying common factor accounted for the association between smoking, alcohol and illicit drug consumption for the three age groups. Common genetic and shared environmental effects showed substantial continuity. In general, as participants aged, the influence of the shared environment decreased, and genetic effects became more substance specific in their effect.

    Conclusions: The current report answers three important questions in the etiology of substance use. The genetic and environmental risk for substance consumption is partly mediated through a common factor and is partly substance specific. Developmentally, evidence was strongest for stability of common genetic effects, with less evidence for genetic innovation. These processes seem to be the same in males and females.

  • 2.
    Beckman, K.
    et al.
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; St Goran Hosp, Stockholm City Council, Stockholm, Sweden.
    Mittendorfer-Rutz, E.
    Department of Clinical Neuroscience, Insurance Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Almqvist, C
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Runeson, B.
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; St Goran Hosp, Stockholm City Council, Stockholm, Sweden.
    Dahlin, M.
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; St Goran Hosp, Stockholm City Council, Stockholm, Sweden.
    Mental illness and suicide after self-harm among young adults: long-term follow-up of self-harm patients, admitted to hospital care, in a national cohort2016In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 46, no 16, p. 3397-3405Article in journal (Refereed)
    Abstract [en]

    Background: Self-harm among young adults is a common and increasing phenomenon in many parts of the world. The long-term prognosis after self-harm at young age is inadequately known. We aimed to estimate the risk of mental illness and suicide in adult life after self-harm in young adulthood and to identify prognostic factors for adverse outcome.

    Method: We conducted a national population-based matched case-cohort study. Patients aged 18-24 years (n = 13 731) hospitalized after self-harm between 1990 and 2003 and unexposed individuals of the same age (n = 137 310 ) were followed until December 2009. Outcomes were suicide, psychiatric hospitalization and psychotropic medication in short-term (1-5 years) and long-term (>5 years) follow-up.

    Results: Self-harm implied an increased relative risk of suicide during follow-up [hazard ratio (HR) 16.4, 95% confidence interval (CI) 12.9-20.9). At long-term follow-up, 20.3% had psychiatric hospitalizations and 51.1% psychotropic medications, most commonly antidepressants and anxiolytics. There was a six-fold risk of psychiatric hospitalization (HR 6.3, 95% CI 5.8-6.8) and almost three-fold risk of psychotropic medication (HR 2.8, 95% CI 2.7-3.0) in long-term follow-up. Mental disorder at baseline, especially a psychotic disorder, and a family history of suicide were associated with adverse outcome among self-harm patients.

    Conclusion: We found highly increased risks of future mental illness and suicide among young adults after self-harm. A history of a mental disorder was an important indicator of long-term adverse outcome. Clinicians should consider the substantially increased risk of suicide among self-harm patients with psychotic disorders.

  • 3.
    Bramson, L. M.
    et al.
    Indiana University, Bloomington, United States .
    Rickert, M. E.
    Indiana University, Bloomington, United States.
    Class, Q. A.
    University of Chicago, Chicago, United States .
    Sariaslan, A.
    University of Oxford, Oxford, United Kingdom .
    Almqvist, C.
    Karolinska Institutet, Stockholm, Sweden .
    Larsson, Henrik
    Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Karolinska Institutet, Stockholm, Sweden .
    D'Onofrio, B. M.
    Indiana University, Bloomington, United States.
    The association between childhood relocations and subsequent risk of suicide attempt, psychiatric problems, and low academic achievement2016In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 46, no 5, p. 969-979Article in journal (Refereed)
    Abstract [en]

    Background: Given the frequency with which families change residences, the effects of childhood relocations have gained increasing research attention. Many researchers have demonstrated that childhood relocations are associated with a variety of adverse outcomes. However, drawing strong causal claims remains problematic due to uncontrolled confounding factors.

    Method: We utilized longitudinal, population-based Swedish registers to generate a nationally representative sample of offspring born 1983-1997 (n = 1 510 463). Using Cox regression and logistic regression, we examined the risk for numerous adverse outcomes after childhood relocation while controlling for measured covariates. To account for unmeasured genetic and environmental confounds, we also compared differentially exposed cousins and siblings.

    Results: In the cohort baseline model, each annual relocation was associated with risk for the adverse outcomes, including suicide attempt [hazard ratio (HR) 1.19, 95% confidence interval (CI) 1.19-1.20]. However, when accounting for offspring and parental covariates (HR 1.08, 95% CI 1.07-1.09), as well as genetic and environmental confounds shared by cousins (HR 1.07, 95% CI 1.05-1.09) and siblings (HR 1.00, 95% CI 0.97-1.04), the risk for suicide attempt attenuated. We found a commensurate pattern of results for severe mental illness, substance abuse, criminal convictions, and low academic achievement.

    Conclusions: Previous research may have overemphasized the independent association between relocations and later adverse outcomes. The results suggest that the association between childhood relocations and suicide attempt, psychiatric problems, and low academic achievement is partially explained by genetic and environmental confounds correlated with relocations. This study demonstrates the importance of using family-based, quasi-experimental designs to test plausible alternate hypotheses when examining causality.

  • 4.
    Capusan, A. J.
    et al.
    Department of Psychiatry and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Kuja-Halkola, R.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bendtsen, P.
    Department of Medical specialist and Department of Medical and Health Sciences, Linköpings University, Motala, Sweden.
    Viding, E.
    Developmental Risk and Resilience Unit, University College London, London, UK.
    McCrory, E.
    Developmental Risk and Resilience Unit, University College London, London, UK.
    Marteinsdottir, I.
    Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience (CSAN), Linköping University, Linköping, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Childhood maltreatment and attention deficit hyperactivity disorder symptoms in adults: a large twin study2016In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 46, no 12, p. 2637-2646Article in journal (Refereed)
    Abstract [en]

    Background: Childhood maltreatment (CM) has been associated with increased risk of attention deficit hyperactivity disorder (ADHD) in children and adults. It is, however, unclear whether this association is causal or due to familial confounding.

    Method: Data from 18 168 adult twins, aged 20-46 years, were drawn from the population-based Swedish twin registry. Retrospective self-ratings of CM (emotional and physical neglect, physical and sexual abuse and witnessing family violence), and self-ratings for DSM-IV ADHD symptoms in adulthood were analysed. Possible familial confounding was investigated using a within twin-pair design based on monozygotic (MZ) and dizygotic (DZ) twins.

    Results: CM was significantly associated with increased levels of ADHD symptom scores in adults [regression coefficient: 0.40 standard deviations, 95% confidence interval (CI) 0.37-0.43]. Within twin-pair analyses showed attenuated but significant estimates within DZ (0.29, 95% CI 0.21-0.36) and MZ (0.18, 95% CI 0.10-0.25) twin pairs. Similar results emerged for hyperactive/impulsive and inattentive ADHD symptom scores separately in association with CM. We conducted sensitivity analyses for early maltreatment, before age 7, and for abuse and neglect separately, and found similarly reduced estimates in DZ and MZ pairs. Re-traumatization after age 7 did not significantly influence results.

    Conclusions: CM was significantly associated with increased ADHD symptoms in adults. Associations were partly due to familial confounding, but also consistent with a causal interpretation. Our findings support cognitive neuroscience studies investigating neural pathways through which exposure to CM may influence ADHD. Clinicians treating adults with ADHD should be aware of the association with maltreatment.

  • 5.
    Capusan, A. J.
    et al.
    Department of Psychiatry and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden; Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience (CSAN), Linköping University, Linköping, Sweden.
    Yao, S.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, R.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bulik, C. M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, USA; Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, USA.
    Thornton, L. M.
    Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, USA.
    Bendtsen, P.
    Department of Medical Specialist and Department of Medical and Health Sciences, Linköping University, Motala, Sweden.
    Marteinsdottir, I.
    Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience (CSAN), Linköping University, Linköping, Sweden.
    Thorsell, A.
    Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience (CSAN), Linköping University, Linköping, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Genetic and environmental aspects in the association between attention-deficit hyperactivity disorder symptoms and binge-eating behavior in adults: a twin study2017In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 47, no 16, p. 2866-2878Article in journal (Refereed)
    Abstract [en]

    Background: Prior research demonstrated that attention-deficit hyperactivity disorder (ADHD) is associated with binge-eating behavior, binge-eating disorder (BED), and bulimia nervosa (BN). The aim of this study was to investigate these associations in an adult twin population, and to determine the extent to which ADHD symptoms and binge-eating behavior share genetic and environmental factors.

    Methods: We used self-reports of current ADHD symptoms and lifetime binge-eating behavior and associated characteristics from a sample of over 18 000 adult twins aged 20-46 years, from the population-based Swedish Twin Registry. Mixed-effects logistic regression was used to examine the association between ADHD and lifetime binge-eating behavior, BED, and BN. Structural equation modeling was used in 13 773 female twins to determine the relative contribution of genetic and environmental factors to the association between ADHD symptoms and binge-eating behavior in female adult twins.

    Results: ADHD symptoms were significantly associated with lifetime binge-eating behavior, BED, and BN. The heritability estimate for current ADHD symptoms was 0.42 [95% confidence interval (CI) 0.41-0.44], and for lifetime binge-eating behavior 0.65 (95% CI 0.54-0.74). The genetic correlation was estimated as 0.35 (95% CI 0.25-0.46) and the covariance between ADHD and binge-eating behavior was primarily explained by genetic factors (91%). Non-shared environmental factors explained the remaining part of the covariance.

    Conclusions: The association between adult ADHD symptoms and binge-eating behavior in females is largely explained by shared genetic risk factors.

  • 6.
    Cesta, Carolyn E.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre for Pharmacoepidemiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Öberg, Anna S.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
    Ibrahimson, Abraham
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Yusuf, Ikram
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA.
    Bulik, Cynthia M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
    Fernández de la Cruz, Lorena
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Mataix-Cols, David
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Landén, Mikael
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
    Rosenqvist, Mina A.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Maternal polycystic ovary syndrome and risk of neuropsychiatric disorders in offspring: prenatal androgen exposure or genetic confounding?2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, p. 1-9Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Maternal polycystic ovary syndrome (PCOS) has been proposed as a model for investigating the role of prenatal androgen exposure in the development of neuropsychiatric disorders. However, women with PCOS are at higher risk of developing psychiatric conditions and previous studies are likely confounded by genetic influences.

    METHODS: A Swedish nationwide register-based cohort study was conducted to disentangle the influence of prenatal androgen exposure from familial confounding in the association between maternal PCOS and offspring attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and Tourette's disorder and chronic tic disorders (TD/CTD). PCOS-exposed offspring (n = 21 280) were compared with unrelated PCOS-unexposed offspring (n = 200 816) and PCOS-unexposed cousins (n = 17 295). Associations were estimated with stratified Cox regression models.

    RESULTS: PCOS-exposed offspring had increased risk of being diagnosed with ADHD, ASD, and TD/CTD compared with unrelated PCOS-unexposed offspring. Associations were stronger in girls for ADHD and ASD but not TD/CTD [ADHD: adjusted hazard ratio (aHR) = 1.61 (95% confidence interval (CI) 1.31-1.99), ASD: aHR = 2.02 (95% CI 1.45-2.82)] than boys [ADHD: aHR = 1.37 (95% CI 1.19-1.57), ASD: aHR = 1.46 (95% CI 1.21-1.76)]. For ADHD and ASD, aHRs for girls were stronger when compared with PCOS-unexposed cousins, but slightly attenuated for boys.

    CONCLUSIONS: Estimates were similar when accounting for familial confounding (i.e. genetics and environmental factors shared by cousins) and stronger in girls for ADHD and ASD, potentially indicating a differential influence of prenatal androgen exposure v. genetic factors. These results strengthen evidence for a potential causal influence of prenatal androgen exposure on the development of male-predominant neuropsychiatric disorders in female offspring of women with PCOS.

  • 7.
    Chen, Qi
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Hartman, Catharina A.
    Department of Psychiatry, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
    Kuja-Halkola, Ralf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Faraone, Stephen V.
    Department of Biomedicine, K.G. Jebsen Centre for Neuropsychiatric Disorders, University of Bergen, Bergen, Norway; Departments of Psychiatry and Neuroscience and Physiology, SUNY Upstate Medical University, New York, USA.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Pediatric Allergy and Pulmonology Unit at Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Attention-deficit/hyperactivity disorder and clinically diagnosed obesity in adolescence and young adulthood: a register-based study in Sweden2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 49, no 11, p. 1841-1849Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: A recent family study of young adult males suggests a shared familial liability between attention-deficit/hyperactivity disorder (ADHD) and high body mass index (BMI), and a genome-wide meta-analysis reported a genetic correlation of 0.26 between ADHD and BMI. To date, it is unclear whether these findings generalize to the relationship between ADHD and clinically diagnosed obesity.

    METHOD: By linking the Swedish national registers, we identified 25 38 127 individuals born between 1973 and 2000, together with their siblings and cousins. The risk of clinical obesity in individuals with ADHD was compared with the risk in those without ADHD. The relative contributions of genetic and environmental factors to the association between ADHD and clinical obesity were examined via assessment of the familial co-aggregation of the two conditions and quantitative genetic analysis.

    RESULTS: Individuals with ADHD were at an increased risk of clinical obesity compared with those without (risk difference 3.73%, 95% confidence interval (CI) 3.55-3.90%; risk ratio 3.05, 95% CI 2.95-3.15). Familial co-aggregation of ADHD and clinical obesity was detected and the strength of the co-aggregation decreased by decreasing genetic relatedness. The correlation between the liabilities to ADHD and clinical obesity can be entirely attributed to their genetic correlation (rg 0.30, 95% CI 0.17-0.44).

    CONCLUSION: The association between ADHD and clinical obesity in adolescence and young adulthood can be entirely attributed to genetic underpinnings shared by the two conditions. Children with ADHD should be monitored for weight gain so that preventive measures can be taken for those on a suboptimal trajectory.

  • 8.
    Class, Q. A.
    et al.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, United States.
    Abel, K. M.
    Centre for Women's Mental Health, Manchester Academic Health Sciences, University of Manchester, Manchester, United Kingdom .
    Khashan, A. S.
    Anu Research Centre, Department of Obstetrics and Gynaecology, University College Cork, Cork, Ireland .
    Rickert, M. E.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, United States.
    Dalman, C.
    Department of Public Health Sciences, Division of Public Health Epidemiology, Karolinska Institutet, Stockholm, Sweden .
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Hultman, C. M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Långström, N.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    D'Onofrio, B. M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, United States.
    Offspring psychopathology following preconception, prenatal and postnatal maternal bereavement stress2014In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 44, no 1, p. 71-84Article in journal (Refereed)
    Abstract [en]

    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.

  • 9. Furmark, Tomas
    et al.
    Tillfors, M.
    Stattin, Håkan
    Örebro University, Department of Behavioural, Social and Legal Sciences.
    Ekselius, L.
    Fredrikson, M.
    Social phobia subtypes in the general population revealed by cluster analysis2000In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 30, no 6, p. 1335-1344Article in journal (Refereed)
    Abstract [en]

    Background.

    Epidemiological data on subtypes of social phobia are scarce and their defining features are debated. Hence, the present study explored the prevalence and descriptive characteristics of empirically derived social phobia subgroups in the general population.

    Methods.

    To reveal subtypes, data on social distress, functional impairment, number of social fears and criteria fulfilled for avoidant personality disorder were extracted from a previously published epidemiological study of 188 social phobics and entered into an hierarchical cluster analysis. Criterion validity was evaluated by comparing clusters on the Social Phobia Scale (SPS) and the Social Interaction Anxiety Scale (SIAS). Finally, profile analyses were performed in which clusters were compared on a set of sociodemographic and descriptive characteristics.

    Results.

    Three clusters emerged, consisting of phobics scoring either high (generalized subtype), intermediate (non-generalized subtype) or low (discrete subtype) on all variables. Point prevalence rates were 2.0%, 5.9% and 7.7% respectively. All subtypes were distinguished on both SPS and SIAS. Generalized or severe social phobia tended to be over-represented among individuals with low levels of educational attainment and social support. Overall, public-speaking was the most common fear.

    Conclusions.

    Although categorical distinctions may be used, the present data suggest that social phobia subtypes in the general population mainly differ dimensionally along a mild-moderate-severe continuum, and that the number of cases declines with increasing severity.

  • 10.
    Ghirardi, Laura
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Pettersson, Erik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Taylor, Mark J.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Freitag, Christine M.
    Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, Goethe University, Frankfurt am Main, Germany.
    Franke, Barbara
    Department of Human Genetics and Psychiatry, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands.
    Asherson, Philip
    Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology, and Neuroscience, King’s College London, London, UK.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, Ralf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Genetic and environmental contribution to the overlap between ADHD and ASD trait dimensions in young adults: a twin study2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 49, no 10, p. 1713-1721Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Traits of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are strongly associated in children and adolescents, largely due to genetic factors. Less is known about the phenotypic and aetiological overlap between ADHD and ASD traits in adults.

    METHODS: We studied 6866 individuals aged 20-28 years from the Swedish Study of Young Adult Twins. Inattention (IA) and hyperactivity/impulsivity (HI) were assessed using the WHO Adult ADHD Self-Report Scale-V1.1. Repetitive and restricted behaviours (RRB) and social interaction and communication (SIC) were assessed using the Autism-Tics, ADHD, and other Comorbidities inventory. We used structural equation modelling to decompose covariance between these ADHD and ASD trait dimensions into genetic and shared/non-shared environmental components.

    RESULTS: At the phenotypic level, IA was similarly correlated with RRB (r = 0.33; 95% Confidence Interval (CI) 0.31-0.36) and with SIC (r = 0.32; 95% CI 0.29-0.34), whereas HI was more strongly associated with RRB (r = 0.38; 95% CI 0.35-0.40) than with SIC (r = 0.24; 95% CI 0.21-0.26). Genetic and non-shared environmental effects accounted for similar proportions of the phenotypic correlations, whereas shared environmental effects were of minimal importance. The highest genetic correlation was between HI and RRB (r = 0.56; 95% 0.46-0.65), and the lowest was between HI and SIC (r = 0.33; 95% CI 0.23-0.43).

    CONCLUSIONS: We found evidence for dimension-specific phenotypic and aetiological overlap between ADHD and ASD traits in adults. Future studies investigating mechanisms underlying comorbidity between ADHD and ASD may benefit from exploring several symptom-dimensions, rather than considering only broad diagnostic categories.

  • 11.
    Hesser, Hugo
    et al.
    Department of Behavioural Sciences and Learning, Linköping University, Linköping, Sweden.
    Hedman, E.
    Department of Clinical Neuroscience, Division of Psychology, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Neuroscience, Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lindfors, P.
    Department of Internal Medicine Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, Sweden; Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Andersson, E.
    Department of Clinical Neuroscience, Division of Psychology, Karolinska Institutet, Stockholm, Sweden.
    Ljótsson, B.
    Department of Clinical Neuroscience, Division of Psychology, Karolinska Institutet, Stockholm, Sweden.
    The specific effect of systematic exposure in irritable bowel syndrome: Complier average causal effect analysis using growth mixture modeling2017In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 47, no 15, p. 2653-2662Article in journal (Refereed)
    Abstract [en]

    Background: We reanalyzed data from a previously published randomized component study that aimed to test the incremental effect of systematic exposure in an internet-delivered cognitive behavioral treatment (ICBT) for irritable bowel syndrome (IBS).

    Methods: Three hundred and nine individuals with IBS were randomly assigned to either the full treatment protocol (experimental condition) or the same treatment protocol without systematic exposure (control). Participants were assessed weekly for IBS symptoms over the active treatment phase. We used a complier average causal effect (CACE) analysis, in the growth mixture modeling framework, to (1) examine the specific effect of exposure among those who received the intervention (i.e. compliers), and (2) explore the associations of pre-treatment patient characteristics with compliance status and outcome changes.

    Results: Fifty-five per cent of those assigned to the experimental condition were classified as compliers. The CACE analysis that took into account compliance status demonstrated that the magnitude of the incremental effect of systematic exposure on IBS symptoms was larger than the effect observed in an intention-to-treat analysis that ignored compliance status (d = 0.81 v. d = 0.44). Patients with university education showed more improvement during the exposure phase of the treatment. Pre-treatment patient characteristics did not predict compliance status.

    Conclusions: The effect of systematic exposure on IBS symptoms is of substantial magnitude among those individuals who actually receive the intervention (CACE). Studying the subsample of individuals who discontinue treatment prematurely and tailoring interventions to improve compliance may increase overall improvement rates in ICBT for IBS.

  • 12.
    Hirvikoski, T.
    et al.
    Department of Women's and Children's Health, Pediatric Neuropsychiatry Unit, Center for Neurodevelopmental Disorders at Karolinska Institutet (KIND), Karolinska Institutet, Stockholm, Sweden; Habilitation & Health, Stockholm County Council, Stockholm, Sweden; Center for Psychiatry Research, Stockholm County Council, Stockholm, Sweden .
    Boman, M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Chen, Q.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, B. M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University Bloomington, Bloomington, Indiana, USA.
    Mittendorfer-Rutz, E.
    Department of Clinical Neuroscience, Division of Insurance Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bölte, S.
    Department of Women's and Children's Health, Pediatric Neuropsychiatry Unit, Center for Neurodevelopmental Disorders at Karolinska Institutet (KIND), Karolinska Institutet, Stockholm, Sweden; Center for Psychiatry Research, Stockholm County Council, Stockholm, Sweden; Child and Adolescent Psychiatry, Stockholm County Council, Stockholm, Sweden.
    Larsson, H.
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; .
    Individual risk and familial liability for suicide attempt and suicide in autism: a population-based study2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, p. 1-12Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Studies on the individual gender-specific risk and familial co-aggregation of suicidal behaviour in autism spectrum disorder (ASD) are lacking.

    METHODS: We conducted a matched case-cohort study applying conditional logistic regression models on 54 168 individuals recorded in 1987-2013 with ASD in Swedish national registers: ASD without ID n = 43 570 (out of which n = 19035, 43.69% with ADHD); ASD + ID n = 10 598 (out of which n = 2894 individuals, 27.31% with ADHD), and 270 840 controls, as well as 347 155 relatives of individuals with ASD and 1 735 775 control relatives.

    RESULTS: The risk for suicidal behaviours [reported as odds ratio OR (95% confidence interval CI)] was most increased in the ASD without ID group with comorbid ADHD [suicide attempt 7.25 (6.79-7.73); most severe attempts i.e. requiring inpatient stay 12.37 (11.33-13.52); suicide 13.09 (8.54-20.08)]. The risk was also increased in ASD + ID group [all suicide attempts 2.60 (2.31-2.92); inpatient only 3.45 (2.96-4.02); suicide 2.31 (1.16-4.57)]. Females with ASD without ID had generally higher risk for suicidal behaviours than males, while both genders had highest risk in the case of comorbid ADHD [females, suicide attempts 10.27 (9.27-11.37); inpatient only 13.42 (11.87-15.18); suicide 14.26 (6.03-33.72); males, suicide attempts 5.55 (5.10-6.05); inpatient only 11.33 (9.98-12.86); suicide 12.72 (7.77-20.82)]. Adjustment for psychiatric comorbidity attenuated the risk estimates. In comparison to controls, relatives of individuals with ASD also had an increased risk of suicidal behaviour.

    CONCLUSIONS: Clinicians treating patients with ASD should be vigilant for suicidal behaviour and consider treatment of psychiatric comorbidity.

  • 13.
    Isomura, K
    et al.
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Boman, M
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Rück, C
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Serlachius, E
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Mataix-Cols, D
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Population-based, multi-generational family clustering study of social anxiety disorder and avoidant personality disorder2015In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 45, no 8, p. 1581-1589Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: We aimed to provide unbiased estimates of familial risk and heritability of social anxiety disorder (SAD) and avoidant personality disorder (AVPD).

    METHOD: We identified 18 399 individuals diagnosed with SAD and 2673 with AVPD in the Swedish National Patient Register between 1997 and 2009. Risks (odds ratios; OR) for SAD in all biological and non-biological relatives of probands, compared to relatives of unaffected individuals were calculated. We also estimated the risks for AVPD in relatives of probands with SAD.

    RESULTS: The risk for SAD among relatives of SAD probands increased proportionally to the degree of genetic relatedness. The risks for first-degree relatives [OR 4.74, 95% confidence interval (CI) 4.28-5.25] were significantly higher than for second-degree and third-degree relatives. Second-degree relatives (OR 2.30, 95% CI 2.01-2.63) had significantly higher risk than third-degree relatives (OR 1.72, 95% CI 1.52-1.94). Relatives at similar genetic distances had similar risks for SAD, despite different degrees of shared environment. Heritability was estimated to be approximately 56%. There were no significant sex differences in the familial patterns. The risk of AVPD in relatives of SAD probands was significantly elevated, even after excluding individuals with both diagnoses (first-degree OR 3.54, second-degree OR 2.20, third-degree OR 1.62). Non-biological relatives (spouses/partners) also had elevated risks for both SAD (OR 4.01) and AVPD (OR 3.85).

    CONCLUSIONS: SAD clusters in families primarily due to genetic factors. SAD and AVPD are aetiologically related and may represent different expressions of the same vulnerability. The strong marital concordance observed in SAD/AVPD may indicate assortative mating but the exact mechanisms and implications require further investigation.

  • 14.
    Javaras, K N
    et al.
    Department of Psychiatry, University of North Carolina, Chapel Hill NC, USA.
    Rickert, M E
    Department of Psychological and Brain Sciences, Indiana University, Bloomington IN, USA.
    Thornton, L M
    Department of Psychiatry, University of North Carolina, Chapel Hill NC, USA.
    Peat, C M
    Department of Psychiatry, University of North Carolina, Chapel Hill NC, USA; Department of Neurosurgery, University of North Carolina, Chapel Hill NC, USA.
    Baker, J H
    Department of Psychiatry, University of North Carolina, Chapel Hill NC, USA.
    Birgegård, A
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Norring, C
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Landén, M
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Almqvist, C
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children’ s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bulik, C M
    Department of Psychiatry, University of North Carolina, Chapel Hill NC, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Nutrition, University of North Carolina, Chapel Hill NC, USA.
    D'Onofrio, B M
    Department of Psychological and Brain Sciences, Indiana University, Bloomington IN, USA.
    Paternal age at childbirth and eating disorders in offspring2017In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 47, no 3, p. 576-584Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Advanced paternal age at childbirth is associated with psychiatric disorders in offspring, including schizophrenia, bipolar disorder and autism. However, few studies have investigated paternal age's relationship with eating disorders in offspring. In a large, population-based cohort, we examined the association between paternal age and offspring eating disorders, and whether that association remains after adjustment for potential confounders (e.g. parental education level) that may be related to late/early selection into fatherhood and to eating disorder incidence.

    METHOD: Data for 2 276 809 individuals born in Sweden 1979-2001 were extracted from Swedish population and healthcare registers. The authors used Cox proportional hazards models to examine the effect of paternal age on the first incidence of healthcare-recorded anorexia nervosa (AN) and all eating disorders (AED) occurring 1987-2009. Models were adjusted for sex, birth order, maternal age at childbirth, and maternal and paternal covariates including country of birth, highest education level, and lifetime psychiatric and criminal history.

    RESULTS: Even after adjustment for covariates including maternal age, advanced paternal age was associated with increased risk, and younger paternal age with decreased risk, of AN and AED. For example, the fully adjusted hazard ratio for the 45+ years (v. the 25-29 years) paternal age category was 1.32 [95% confidence interval (CI) 1.14-1.53] for AN and 1.26 (95% CI 1.13-1.40) for AED.

    CONCLUSIONS: In this large, population-based cohort, paternal age at childbirth was positively associated with eating disorders in offspring, even after adjustment for potential confounders. Future research should further explore potential explanations for the association, including de novo mutations in the paternal germline.

  • 15.
    Kendler, K S
    et al.
    Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia, Virginia Commonwealth University, Richmond VA, USA; Department of Psychiatry, Medical College of Virginia, Virginia Commonwealth University, Richmond VA, USA; Department of Human and Molecular Genetics, Medical College of Virginia, Virginia Commonwealth University, Richmond VA, USA.
    Patrick, C J
    Department of Psychology, Florida State University, Tallahassee FL, USA.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Karolinska Institute Center for Neurodevelopmental Disorders, Stockholm, Sweden.
    Gardner, C O
    Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia, Virginia Commonwealth University, Richmond VA, USA; Department of Psychiatry, Medical College of Virginia, Virginia Commonwealth University, Richmond VA, USA.
    Lichtenstein, P
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Genetic and environmental risk factors in males for self-report externalizing traits in mid-adolescence and criminal behavior through young adulthood2013In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 43, no 10, p. 2161-2168Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Externalizing traits or behaviors are typically assessed by self-report scales or criminal records. Few genetically informative studies have used both methods to determine whether they assess the same genetic or environmental risk factors.

    METHOD: We examined 442 male Swedish twin pairs with self-reported externalizing behaviors at age 16–17 years [externalizing traits (EXT), self-reported delinquency (SRD), impulsivity (IMP), grandiosity (GRD) and callousness (CLS)] and criminal behavior (CB) from the National Suspect Registry from age 13 to 25 years. Multivariate structural equation modeling was conducted with Mx.

    RESULTS: The best-fit model contained one genetic, one shared environmental and two non-shared environmental common factors, and variable specific genetic and non-shared environmental factors. The risk for CB was influenced substantially by both genetic (a2=0.48) and familial–environmental factors (c2=0.22). About one-third of the genetic risk for CB but all of the shared environmental risk was indexed by the self-report measures. The degree to which the individual measures reflected genetic versus familial–environmental risks for CB varied widely. GRD and CLS were correlated with CB mainly through common genetic risk factors. SRD and CB covaried largely because of shared familial–environmental factors. For EXT and IMP, observed correlations with CB resulted in about equal parts from shared genetic and shared familial–environmental factors.

    CONCLUSIONS: In adolescence, measures of grandiose and callous temperament best tap the genetic liability to CB.Measures of antisocial behaviors better index familial–environmental risks for CB. A substantial proportion of the genetic risk to CB was not well reflected in any of the self-report measures.

  • 16.
    Khemiri, L
    et al.
    Department of Clinical Neuroscience, Centre for Psychiatric Research, Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, R
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Jayaram-Lindström, N
    Department of Clinical Neuroscience, Centre for Psychiatric Research, Karolinska Institutet, Stockholm, Sweden.
    Genetic overlap between impulsivity and alcohol dependence: a large-scale national twin study2016In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 46, no 5, p. 1091-1102Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Alcohol dependence is associated with increased levels of impulsivity, but the genetic and environmental underpinnings of this overlap remain unclear. The purpose of the current study was to investigate the degree to which genetic and environmental factors contribute to the overlap between alcohol dependence and impulsivity.

    METHOD: Univariate and bivariate twin model fitting was conducted for alcohol dependence and impulsivity in a national sample of 16 819 twins born in Sweden from 1959 to 1985.

    RESULTS: The heritability estimate for alcohol dependence was 44% [95% confidence interval (CI) 31-57%] for males and 62% (95% CI 52-72%) for females. For impulsivity, the heritability was 33% (95% CI 30-36%) in males and females. The bivariate twin analysis indicated a statistically significant genetic correlation between alcohol dependence and impulsivity of 0.40 (95% CI 0.23-0.58) in males and 0.20 (95% CI 0.07-0.33) in females. The phenotypic correlation between alcohol dependence and impulsivity was 0.20 and 0.17 for males and females, respectively, and the bivariate heritability was 80% (95% CI 47-117%) for males and 53% (95% CI 19-86%) for females. The remaining variance in all models was accounted for by non-shared environmental factors.

    CONCLUSIONS: The association between alcohol dependence and impulsivity can be partially accounted for by shared genetic factors. The genetic correlation was greater in men compared with women, which may indicate different pathways to the development of alcohol dependence between sexes. The observed genetic overlap has clinical implications regarding treatment and prevention, and partially explains the substantial co-morbidity between alcohol dependence and psychiatric disorders characterized by impulsive behaviour.

  • 17.
    Koffel, E
    et al.
    Center for Chronic Disease Outcomes Research, Minneapolis MN, USA; Minneapolis VA Healthcare System, Minneapolis MN, USA; Department of Psychiatry, University of Minnesota, Minneapolis MN, USA.
    Kramer, Mark
    Minneapolis VA Healthcare System, Minneapolis MN, USA; Department of Psychiatry, University of Minnesota, Minneapolis MN, USA.
    Arbisi, P. A.
    Minneapolis VA Healthcare System, Minneapolis MN, USA; Department of Psychiatry, University of Minnesota, Minneapolis MN, USA; Department of Psychology, University of Minnesota, Minneapolis MN, USA.
    Erbes, C. R.
    Center for Chronic Disease Outcomes Research, Minneapolis MN, USA; Minneapolis VA Healthcare System, Minneapolis MN, USA; Department of Psychiatry, University of Minnesota, Minneapolis MN, USA.
    Kaler, M
    Minneapolis VA Healthcare System, Minneapolis MN, USA.
    Polusny, M. A.
    Center for Chronic Disease Outcomes Research, Minneapolis MN, USA; Minneapolis VA Healthcare System, Minneapolis MN, USA; Department of Psychiatry, University of Minnesota, Minneapolis MN, USA.
    Personality traits and combat exposure as predictors of psychopathology over time2016In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 46, no 1, p. 209-220Article in journal (Refereed)
    Abstract [en]

    Background: Research suggests that personality traits have both direct and indirect effects on the development of psychological symptoms, with indirect effects mediated by stressful or traumatic events. This study models the direct influence of personality traits on residualized changes in internalizing and externalizing symptoms following a stressful and potentially traumatic deployment, as well as the indirect influence of personality on symptom levels mediated by combat exposure.

    Method: We utilized structural equation modeling with a longitudinal prospective study of 522 US National Guard soldiers deployed to Iraq. Analyses were based on self-report measures of personality, combat exposure, and internalizing and externalizing symptoms.

    Results: Both pre-deployment Disconstraint and externalizing symptoms predicted combat exposure, which in turn predicted internalizing and externalizing symptoms. There was a significant indirect effect for pre-deployment externalizing symptoms on post-deployment externalizing via combat exposure (p < 0.01). Negative Emotionality and pre-deployment internalizing symptoms directly predicted post-deployment internalizing symptoms, but both were unrelated to combat exposure. No direct effects of personality on residualized changes in externalizing symptoms were found.

    Conclusions: Baseline symptom dimensions had significant direct and indirect effects on post-deployment symptoms. Controlling for both pre-exposure personality and symptoms, combat experiences remained positively related to both internalizing and externalizing symptoms. Implications for diagnostic classification are discussed.

  • 18.
    Kramer, Mark
    et al.
    Department of Psychology, University of Minnesota, Twin Cities Campus, Minneapolis MN, USA.
    Krueger, R. F.
    Department of Psychology, University of Minnesota, Twin Cities Campus, Minneapolis MN, USA.
    Hicks, B. M.
    Department of Psychology, University of Minnesota, Twin Cities Campus, Minneapolis MN, USA.
    The role of internalizing and externalizing liability factors in accounting for gender differences in the prevalence of common psychopathological syndromes2008In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 38, no 1, p. 51-62Article in journal (Refereed)
    Abstract [en]

    Background: We hypothesized that gender differences in average levels on the internalizing and externalizing factors that account for co-morbidity among common psychopathological syndromes in both men and women account for gender differences in the prevalence of specific syndromes.

    Method: The latent structure of 11 syndromes was examined in a middle-aged (mean age=52.66 years, S.D.=5.82) sample of 2992 (37% men) members of the community-based Minnesota Twin Registry (MTR) assessed using 10 scales of the Psychiatric Diagnostic Screening Questionnaire (PDSQ) and an adult antisocial behavior scale. Confirmatory factorial invariance models were applied to a best-fitting, internalizing-externalizing model.

    Results: A 'strong gender invariance model' fit best, indicating that gender differences in the means of individual syndromes were well accounted for by gender differences in mean levels of internalizing and externalizing. Women exhibited higher mean levels of internalizing (d=0.23) and lower mean levels of externalizing (d=-0.52) than men.

    Conclusions: These findings suggest that risk factors for common mental disorders exhibiting gender differences may influence prevalence at the latent factor level. Future research may benefit from focusing on both the latent factor and individual syndrome levels in explaining gender differences in psychopathology.

  • 19.
    Kramer, Mark
    et al.
    University of Minnesota – Twin Cities, Minneapolis MN, USA.
    Patrick, C. J.
    Florida State University, Department of Psychology, Tallahassee FL, USA.
    Krueger, R. F.
    University of Minnesota – Twin Cities, Minneapolis MN, USA.
    Gasperi, M
    University of Minnesota – Twin Cities, Minneapolis MN, USA.
    Delineating physiologic defensive reactivity in the domain of self report: Phenotypic and etiologic structure of dispositional fear2012In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 42, no 6, p. 1305-1320Article in journal (Refereed)
    Abstract [en]

    Background: Individual differences in fear and fearlessness have been investigated at their extremes in relation to markedly different forms of psychopathology - anxiety disorders and psychopathy, respectively. A documented neural substrate of fear-related traits and disorders is defensive reactivity as reflected in aversive startle potentiation (ASP).

    Method: The current study extended prior work by characterizing, in a sample of adult twins from the community (n=2511), the phenotypic and etiologic structure of self-report measures of fear and fearlessness known to be associated with ASP.

    Results: Analyses revealed a hierarchical structure to the trait fear domain, with an overarching, bipolar fear/fearlessness dimension saturating each measure in this domain, and subfactors labeled 'distress,' 'stimulation seeking' and 'sociability' accounting for additional variance in particular measures. The structure of genetic and non-shared environmental associations among the measures closely mirrored the phenotypic structure of the domain.

    Conclusions: The findings have implications for proposals to reconceptualize psychopathology in neurobiological terms.

  • 20.
    Larsson, Henrik
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center of Neurodevelopmental Disorders, Karolinska Institutet Stockholm, Sweden.
    Asherson, P
    MRC Social Genetic and Developmental Psychiatry, Institute of Psychiatry, King’s College London, London, UK.
    Chang, Z
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ljung, T
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Friedrichs, B
    Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Larsson, J-O
    Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Genetic and environmental influences on adult attention deficit hyperactivity disorder symptoms: a large Swedish population-based study of twins2013In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 43, no 1, p. 197-207Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Attention deficit hyperactivity disorder (ADHD) frequently persists into adulthood. Family and twin studies delineate a disorder with strong genetic influences among children and adolescents based on parent- and teacher-reported data but little is known about the genetic and environmental contribution to DSM-IV ADHD symptoms in adulthood. We therefore aimed to investigate the impact of genetic and environmental influences on the inattentive and hyperactive-impulsive symptoms of ADHD in adults.

    METHOD: Twin methods were applied to self-reported assessments of ADHD symptoms from a large population-based Swedish twin study that included data from 15 198 Swedish male and female twins aged 20 to 46 years.

    RESULTS: The broad heritability [i.e., A + D, where A is an additive genetic factor and D (dominance) a non-additive genetic factor] was 37% (A = 11%, D = 26%) for inattention and 38% (A = 18%, D = 20%) for hyperactivity-impulsivity. The results also indicate that 52% of the phenotypic correlation between inattention and hyperactivity-impulsivity (r = 0.43) was explained by genetic influences whereas the remaining part of the covariance was explained by non-shared environmental influences. These results were replicated across age strata.

    CONCLUSIONS: Our findings of moderate broad heritability estimates are consistent with previous literature on self-rated ADHD symptoms in older children, adolescents and adults and retrospective reports of self-rated childhood ADHD by adults but differ from studies of younger children with informant ratings. Future research needs to clarify whether our data indicate a true decrease in the heritability of ADHD in adults compared to children, or whether this relates to the use of self-ratings in contrast to informant data.

  • 21.
    Larsson, Henrik
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Chang, Z
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, B M
    Department of Psychological and Brain Sciences, Indiana University, Bloomington IN, USA.
    Lichtenstein, P
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    The heritability of clinically diagnosed attention deficit hyperactivity disorder across the lifespan2014In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 44, no 10, p. 2223-2229Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: No prior twin study has explored the heritability of clinically diagnosed attention deficit hyperactivity disorder (ADHD). Such studies are needed to resolve conflicting results regarding the importance of genetic effects for ADHD in adults. We aimed to estimate the relative contribution of genetic and environmental influences for clinically diagnosed ADHD across the lifespan with a specific focus on ADHD in adults.

    METHOD: Information on zygosity and sex was obtained from 59514 twins born between 1959 and 2001 included in the nationwide population-based Swedish Twin Registry. Clinical data for ADHD diagnoses (i.e. stimulant or non-stimulant medication for ADHD) were obtained from the Swedish Prescribed Drug Register (PDR) and from the National Patient Register (i.e. ICD-10 diagnosis of ADHD). Twin methods were applied to clinical data of ADHD diagnoses using structural equation modeling with monozygotic (MZ) and dizygotic (DZ) twins.

    RESULTS: The best-fitting model revealed a high heritability of ADHD [0.88, 95% confidence interval (CI) 0.83-0.92] for the entire sample. However, shared environmental effects were non-significant and of minimal importance. The heritability of ADHD in adults was also substantial (0.72, 95% CI 0.56-0.84).

    CONCLUSIONS: This study shows that the heritability of clinically diagnosed ADHD is high across the lifespan. Our finding of high heritability for clinically diagnosed ADHD in adults indicates that the previous reports of low heritability are best explained by rater effects, and that gene-identification studies of ADHD in adults need to consider pervasiveness (e.g. multiple raters) and developmentally (e.g. childhood-onset criteria) informative data.

  • 22.
    Larsson, Henrik
    et al.
    Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King ’ s College London, UK.
    Tuvblad, Catherine
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Sweden.
    Rijsdijk, Fruhling V.
    Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King ’ s College London, UK.
    Andershed, Henrik
    Örebro University, Department of Behavioural, Social and Legal Sciences.
    Grann, Martin
    Centre for Violence Prevention, Karolinska Institutet, Sweden; Swedish Prison and Probation Service, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Sweden.
    A common genetic factor explains the association between psychopathic personality and antisocial behavior2007In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 37, no 1, p. 15-26Article in journal (Refereed)
    Abstract [en]

    Background: Both psychopathic personality traits and antisocial behavior are influenced by geneticas well as environmental factors. However, little is known about how genetic and environmental factors contribute to the associations between the psychopathic personality traits and antisocial behavior.

    Method: Data were drawn from a longitudinal population-based twin sample including all 1480 twin pairs born in Sweden between May 1985 and December 1986. The twins responded to mailed self-report questionnaires at two occasions: 1999 (twins 13–14 years old), and 2002 (twins 16–17years old).

    Results: A common genetic factor loaded substantially on both psychopathic personality traits and antisocial behavior, whereas a common shared environmental factor loaded exclusively on antisocial behavior.

    Conclusions: The genetic overlap between psychopathic personality traits and antisocial behavior may reflect a genetic vulnerability to externalizing psychopathology. The finding of shared environmental influences only in antisocial behavior suggests an etiological distinction between psychopathic personality dimensions and antisocial behavior. Knowledge about temperamental correlates to antisocial behavior is important for identification of susceptibility genes, as well as for possible prevention through identification of at-risk children early in life

  • 23.
    Ljung, T.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sandin, S.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, B.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Runeson, B.
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Långström, N.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center for Violence Prevention, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Parental schizophrenia and increased offspring suicide risk: exploring the causal hypothesis using cousin comparisons2013In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 43, no 3, p. 581-590Article in journal (Refereed)
    Abstract [en]

    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.

  • 24.
    Ljung, T.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sandin, S.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Långström, N.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Runeson, B.
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Offspring death and subsequent psychiatric morbidity in bereaved parents: addressing mechanisms in a total population cohort2014In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 44, no 9, p. 1897-1887Article in journal (Refereed)
    Abstract [en]

    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.

  • 25.
    Merwood, A.
    et al.
    MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK.
    Greven, C. U.
    MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK; Donders Institute for Brain Cognition and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
    Price, T. S.
    MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK; Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA.
    Rijsdijk, F.
    MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK.
    Kuntsi, J.
    MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK.
    McLoughlin, G.
    MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Neurodevelopmental Disorders, Karolinska Institutet, Stockholm, Sweden.
    Asherson, P. J.
    MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK.
    Different heritabilities but shared etiological influences for parent, teacher and self-ratings of ADHD symptoms: an adolescent twin study2013In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 43, no 9, p. 1973-1984Article in journal (Refereed)
    Abstract [en]

    Background: Parent and teacher ratings of attention deficit hyperactivity disorder (ADHD) symptoms yield high estimates of heritability whereas self-ratings typically yield lower estimates. To understand why, the present study examined the etiological overlap between parent, teacher and self-ratings of ADHD symptoms in a population-based sample of 11-12-year-old twins. Method Participants were from the Twins Early Development Study (TEDS). ADHD symptoms were assessed using the Strengths and Difficulties Questionnaire (SDQ) hyperactivity scale completed by parents, teachers and children. Structural equation modeling was used to examine genetic and environmental contributions to phenotypic variance/covariance.

    Results: The broad-sense heritability of ADHD symptoms was 82% for parent ratings, 60% for teacher ratings and 48% for self-ratings. Post-hoc analyses revealed significantly higher heritability for same-teacher than different-teacher ratings of ADHD (76% v. 49%). A common pathway model best explained the relationship between different informant ratings, with common genetic influences accounting for 84% of the covariance between parent, teacher and self-rated ADHD symptoms. The remaining variance was explained by rater-specific genetic and non-shared environmental influences.

    Conclusions: Despite different heritabilities, there were shared genetic influences for parent, teacher and self-ratings of ADHD symptoms, indicating that different informants rated some of the same aspects of behavior. The low heritability estimated for self-ratings and different-teacher ratings may reflect increased measurement error when different informants rate each twin from a pair, and/or greater non-shared environmental influences. Future studies into the genetic influences on ADHD should incorporate informant data in addition to self-ratings to capture a pervasive, heritable component of ADHD symptomatology.

  • 26.
    Pettersson, E.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Song, J.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Agrawal, A.
    Department of Psychiatry, Washington University in Saint Louis School of Medicine, Saint Louis MO, USA.
    Børglum, A. D.
    Department of Biomedicine, Aarhus University, Aarhus, Denmark; iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark; iSEQ, Centre for Integrative Sequencing, Aarhus University, Aarhus, Denmark.
    Bulik, C. M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; University of North Carolina at Chapel Hill, Chapel Hill NC, USA.
    Daly, M. J.
    Analytic and Translational Genetics Unit (ATGU), Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge Massachusetts, USA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge Massachusetts, USA.
    Davis, L. K.
    Department of Medicine, Division of Genetic Medicine, Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville TN, USA.
    Demontis, D.
    Department of Biomedicine, Aarhus University, Aarhus, Denmark; iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark; iSEQ, Centre for Integrative Sequencing, Aarhus University, Aarhus, Denmark.
    Edenberg, H. J.
    Indiana University School of Medicine, Biochemistry and Molecular Biology, Indianapolis IN, USA; Indiana University School of Medicine, Medical and Molecular Genetics, Indianapolis IN, USA.
    Grove, J.
    Department of Biomedicine, Aarhus University, Aarhus, Denmark; iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark; iSEQ, Centre for Integrative Sequencing, Aarhus University, Aarhus, Denmark; BiRC-Bioinformatics Research Centre, Aarhus University, Aarhus, Denmark.
    Gelernter, J.
    Yale University School of Medicine, Genetics and Neurobiology, New Haven CT, USA; US Department of Veterans Affairs, Psychiatry, West Haven CT, USA; Yale University School of Medicine, Psychiatry, New Haven CT, USA.
    Neale, B. M.
    Analytic and Translational Genetics Unit (ATGU), Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge Massachusetts, USA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge Massachusetts, USA.
    Pardinas, A. F.
    Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, Wales.
    Stahl, E.
    Division of Psychiatric Genomics, Icahn School of Medicine at Mount Sinai, New York NY, USA.
    Walters, J. T. R.
    Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, Wales.
    Walters, R.
    Analytic and Translational Genetics Unit (ATGU), Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge Massachusetts, USA .
    Sullivan, P. F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Genetics and Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill NC, USA.
    Posthuma, D.
    Department of Complex Trait Genetics, Center for Neurogenomics and Cognitive Research (CNCR), Amsterdam Neuroscience, VU University Amsterdam, Amsterdam, The Netherlands; Department of Clinical Genetics, VU University Medical Center (VUMC), Amsterdam, The Netherlands.
    Polderman, T. J. C.
    Department of Complex Trait Genetics, Center for Neurogenomics and Cognitive Research (CNCR), Amsterdam Neuroscience, VU University Amsterdam, Amsterdam, The Netherlands.
    Genetic influences on eight psychiatric disorders based on family data of 4 408 646 full and half-siblings, and genetic data of 333 748 cases and controls (vol 49, pg 351, 2019)2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 49, no 2, p. 351-351Article in journal (Refereed)
  • 27.
    Pettersson, E.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Song, J.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Agrawal, A.
    Department of Psychiatry, Washington University in Saint Louis School of Medicine, Saint Louis, MO, USA.
    Børglum, A. D.
    Department of Biomedicine, Aarhus University, Aarhus, Denmark; iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark; iSEQ, Centre for Integrative Sequencing, Aarhus University, Aarhus, Denmark.
    Bulik, C. M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
    Daly, M. J.
    Analytic and Translational Genetics Unit (ATGU), Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
    Davis, L. K.
    Department of Medicine, Division of Genetic Medicine, Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, TN, USA.
    Demontis, D.
    Department of Biomedicine, Aarhus University, Aarhus, Denmark; iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark; iSEQ, Centre for Integrative Sequencing, Aarhus University, Aarhus, Denmark.
    Edenberg, H. J.
    Indiana University School of Medicine, Biochemistry and Molecular Biology, Indianapolis, IN, USA; Indiana University School of Medicine, Medical and Molecular Genetics, Indianapolis, IN, USA.
    Grove, J.
    Department of Biomedicine, Aarhus University, Aarhus, Denmark; iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark; iSEQ, Centre for Integrative Sequencing, Aarhus University, Aarhus, Denmark; BiRC-Bioinformatics Research Centre, Aarhus University, Aarhus, Denmark.
    Gelernter, J.
    Yale University School of Medicine, Genetics and Neurobiology, New Haven, CT, USA; US Department of Veterans Affairs, Psychiatry, West Haven, CT, USA; Yale University School of Medicine, Psychiatry, New Haven, CT, USA.
    Neale, B. M.
    Analytic and Translational Genetics Unit (ATGU), Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
    Pardiñas, A. F.
    Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, Wales.
    Stahl, E.
    Walters, J. T. R.
    Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, Wales, UK.
    Walters, R.
    Analytic and Translational Genetics Unit (ATGU), Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
    Sullivan, P F
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Genetics and Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
    Posthuma, D.
    Department of Complex Trait Genetics, Center for Neurogenomics and Cognitive Research (CNCR), Amsterdam Neuroscience, VU University Amsterdam, Amsterdam, The Netherlands; Department of Clinical Genetics, VU University Medical Center (VUMC), Amsterdam, The Netherlands.
    Polderman, T. J. C.
    Department of Complex Trait Genetics, Center for Neurogenomics and Cognitive Research (CNCR), Amsterdam Neuroscience, VU University Amsterdam, Amsterdam, The Netherlands.
    Genetic influences on eight psychiatric disorders based on family data of 4 408 646 full and half-siblings, and genetic data of 333 748 cases and controls2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 49, no 7, p. 1166-1173Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Most studies underline the contribution of heritable factors for psychiatric disorders. However, heritability estimates depend on the population under study, diagnostic instruments, and study designs that each has its inherent assumptions, strengths, and biases. We aim to test the homogeneity in heritability estimates between two powerful, and state of the art study designs for eight psychiatric disorders.

    METHODS: We assessed heritability based on data of Swedish siblings (N = 4 408 646 full and maternal half-siblings), and based on summary data of eight samples with measured genotypes (N = 125 533 cases and 208 215 controls). All data were based on standard diagnostic criteria. Eight psychiatric disorders were studied: (1) alcohol dependence (AD), (2) anorexia nervosa, (3) attention deficit/hyperactivity disorder (ADHD), (4) autism spectrum disorder, (5) bipolar disorder, (6) major depressive disorder, (7) obsessive-compulsive disorder (OCD), and (8) schizophrenia.

    RESULTS: Heritability estimates from sibling data varied from 0.30 for Major Depression to 0.80 for ADHD. The estimates based on the measured genotypes were lower, ranging from 0.10 for AD to 0.28 for OCD, but were significant, and correlated positively (0.19) with national sibling-based estimates. When removing OCD from the data the correlation increased to 0.50.

    CONCLUSIONS: Given the unique character of each study design, the convergent findings for these eight psychiatric conditions suggest that heritability estimates are robust across different methods. The findings also highlight large differences in genetic and environmental influences between psychiatric disorders, providing future directions for etiological psychiatric research.

  • 28.
    Schaumberg, Katherine
    et al.
    Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
    Jangmo, Andreas
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet,Stockholm, Sweden.
    Thornton, Laura M.
    Department of Psychiatry, University of North Carolina at Chapel Hill,Chapel Hill, NC,USA.
    Birgegård, Andreas
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet and Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Norring, Claes
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet and Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bulik, Cynthia M.
    Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
    Patterns of diagnostic transition in eating disorders: a longitudinal population study in Sweden2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 49, no 5, p. 819-827Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Transition across eating disorder diagnoses is common, reflecting instability of specific eating disorder presentations. Previous studies have examined temporal stability of diagnoses in adult treatment-seeking samples but have not uniformly captured initial presentation for treatment. The current study examines transitions across eating disorder diagnostic categories in a large, treatment-seeking sample of individuals born in Sweden and compares these transitions across two birth cohorts and from initial diagnosis.

    METHODS: Data from Swedish eating disorders quality registers were extracted in 2013, including 9622 individuals who were seen at least twice from 1999 to 2013. Patterns of remission were examined in the entire sample and subsequently compared across initial diagnoses. An older (born prior to 1990) and younger birth cohort were also identified, and analyses compared these cohorts on patterns of diagnostic transition.

    RESULTS: Although diagnostic instability was common, transition between threshold eating disorder diagnoses was infrequent. For all diagnoses, transition to remission was likely to occur following a diagnosis state that matched initial diagnosis, or through a subthreshold diagnostic state. Individuals in the younger cohort were more likely to transition to a state of remission than those in the older cohort.

    CONCLUSIONS: Results indicate more temporal continuity in eating disorder presentations than suggested by previous research and highlight the importance of early detection and intervention in achieving remission.

  • 29.
    Strand, Susanne
    et al.
    Sundsvall Forensic Psychiatric Hospital, Mid-Sweden University, Sundsvall, Sweden.
    McEwan, T. E.
    Centre for Forensic Behavioural Science, Monash University, Melbourne, Australia; The Victorian Institute of Forensic Mental Health, Fairfield, Australia.
    Violence among female stalkers2012In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 42, no 3, p. 545-555Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Female stalkers account for 10-25% of all stalking cases, yet little is known about risk factors for female stalking violence. This study identifies risk factors for female stalking violence and contrasts these with risk factors for male stalking violence.

    METHOD: Seventy-one female and 479 male stalkers presenting to police in Sweden and a specialist stalking clinic in Australia were investigated. Univariate comparisons of behaviour by gender, and comparisons between violent and non-violent female stalkers, were undertaken. Logistic regression was then used to develop a predictive model for stalking violence based on demographic, offence and clinical characteristics.

    RESULTS: Rates of violence were not significantly different between genders (31% of males and 23% of females). For both men and women, violence was associated with a combination of a prior intimate relationship with the victim, threats and approach behaviour. This model produced receiver operating characteristic (ROC) curves with area under the curve (AUC)=0.80 for female stalkers and AUC=0.78 for male stalkers. The most notable gender difference was significantly higher rates of personality disorder among women. High rates of psychotic disorder were found in both genders. Stalking violence was directly related to psychotic symptoms for a small number of women.

    CONCLUSIONS: Similar risk factors generally predict stalking violence between genders, providing initial support for a similar approach to risk assessment for all stalkers. The most notable gender difference was the prevalence of personality and psychotic disorders among female stalkers, supporting an argument for routine psychiatric assessment of women charged with stalking.

  • 30.
    Tuvblad, Catherine
    et al.
    Department of Psychology, University of Southern California CA, USA.
    Wang, Pan
    University of California Los Angeles, Center for Health Policy Research CA, USA.
    Patrick, Christopher J
    Department of Psychology, Florida State University FL, USA.
    Berntsen, Leslie
    Department of Psychology, University of Southern California CA, USA.
    Raine, Adrian
    Departments of Criminology, Psychiatry, and Psychology, University of Pennsylvania, Philadelphia PA, USA.
    Baker, Laura A
    Department of Psychology, University of Southern California CA, USA.
    Genetic and environmental influences on disinhibition, boldness, and meanness as assessed by the triarchic psychopathy measure in 19-20-year-old twins2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 49, no 9, p. 1500-1509Article in journal (Refereed)
    Abstract [en]

    Background: The Triarchic Psychopathy Measure (TriPM) provides Disinhibition, Boldness, and Meanness scales for assessing the three trait domains of the triarchic model. Here we examined the genetic and environmental etiology of these three domains, including evaluation of potential sex differences.

    Methods: A total of 1016 men and women ages 19–20 years were drawn from the University of Southern California Risk Factors for Antisocial Behavior twin study.

    Results: Scores for the three TriPM scales were correlated to differing degrees, with the strongest phenotypic correlation between Disinhibition and Meanness. No sex differences were found in the genetic and environmental influences underlying these three domains, suggesting that the same genes and life experiences contribute to these traits in young men and women. For TriPM Disinhibition and Boldness, genetic factors explained about half or less of the variance, with the rest of the variance being explained by non-shared environmental factors. For TriPM Meanness, on the other hand, genetic, shared environmental, and non-shared environmental factors accounted for the variance. The phenotypic correlation between Disinhibition and Meanness was explained in part by common genes (26%), with the remainder attributable about equally to common shared (39%), and non-shared environmental influences (35%).

    Conclusions: These findings contribute to our understanding of psychopathic personality traits by demonstrating the importance of heritable factors for disinhibition and boldness facets of psychopathy, and the importance of shared environmental influences for the meanness facet.

  • 31.
    Venables, N. C.
    et al.
    Department of Psychology, Florida State University, Tallahassee FL, USA.
    Yancey, J. R.
    Department of Psychology, Florida State University, Tallahassee FL, USA.
    Kramer, Mark
    Minneapolis Veterans Affairs Health Care System and Center for Chronic Disease Outcomes Research, Minneapolis MN, USA.
    Hicks, B. M.
    Department of Psychiatry, University of Michigan, Ann Arbor MI, USA.
    Krueger, R. F.
    Department of Psychology, University of Minnesota, Minneapolis MN, USA.
    Iacono, W. G.
    Department of Psychology, University of Minnesota, Minneapolis MN, USA.
    Joiner, T. E.
    Department of Psychology, Florida State University, Tallahassee FL, USA.
    Patrick, C. J.
    Department of Psychology, Florida State University, Tallahassee FL, USA.
    Psychoneurometric assessment of dispositional liabilities for suicidal behavior: Phenotypic and etiological associations2018In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, Vol. 48, no 3, p. 463-472Article in journal (Refereed)
    Abstract [en]

    Background: Can core genetic liabilities for suicidal behavior be indexed using psychological and neural indicators combined? The current work addressed this question by examining phenotypic and genetic associations of two biobehavioral traits, threat sensitivity (THT) and disinhibition (DIS) - operationalized as psychoneurometric variables (i.e., composites of psychological-scale and neurophysiological measures) - with suicidal behaviors in a sample of adult twins.

    Methods: Participants were 444 identical and fraternal twins recruited from an urban community. THT was assessed using a psychological-scale measure of fear/fearlessness combined with physiological indicators of reactivity to aversive pictures, and DIS was assessed using scale measures of disinhibitory tendencies combined with indicators of brain response from lab performance tasks. Suicidality was assessed using items from structured interview and questionnaire protocols.

    Results: THT and DIS each contributed uniquely to prediction of suicidality when assessed psychoneurometrically (i.e., as composites of scale and neurophysiological indicators). In addition, these traits predicted suicidality interactively, with participants high on both reporting the greatest degree of suicidal behaviors. Biometric (twin-modeling) analyses revealed that a high percentage of the predictive association for each psychoneurometric trait (83% for THT, 68% for DIS) was attributable to genetic variance in common with suicidality.

    Conclusions: Findings indicate that psychoneurometric assessments of biobehavioral traits index genetic liability for suicidal behavior, and as such, can serve as innovative targets for research on core biological processes contributing to severe psychopathology, including suicidal proclivities and actions.

  • 32.
    Vilaplana-Pérez, Alba
    et al.
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden; Departament de Personalitat, Avaluació i Tractaments Psicològics, Universitat de València, València, Spain.
    Pérez-Vigil, Ana
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden; Department of Child and Adolescent Psychiatry and Psychology, Institute of Neuroscience, Hospital Clínic de Barcelona, Barcelona, Spain.
    Sidorchuk, Anna
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
    Brander, Gustaf
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
    Isomura, Kayoko
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
    Hesselmark, Eva
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
    Kuja-Halkola, Ralf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Mataix-Cols, David
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
    Fernández de la Cruz, Lorena
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
    Much more than just shyness: the impact of social anxiety disorder on educational performance across the lifespan2020In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Social anxiety disorder (SAD) has been linked to academic underachievement, but previous studies had methodological limitations. We investigated the association between SAD and objective indicators of educational performance, controlling for a number of covariates and unmeasured confounders shared between siblings.

    METHODS: This population-based birth cohort study included 2 238 837 individuals born in Sweden between 1973 and 1997, followed-up until 2013. Within the cohort, 15 755 individuals had a recorded ICD-10 diagnosis of SAD in the Swedish National Patient Register. Logistic regression models tested the association between SAD and educational performance. We also identified 6488 families with full siblings discordant for SAD.

    RESULTS: Compared to unexposed individuals, individuals diagnosed with SAD were less likely to pass all subjects in the last year of compulsory education [adjusted odds ratios (aOR) ranging from 0.19 to 0.44] and less likely to be eligible for a vocational or academic programme in upper secondary education [aOR = 0.31 (95% confidence interval [CI] 0.30-0.33) and aOR = 0.52 (95% CI 0.50-0.55), respectively], finish upper secondary education [aOR = 0.19 (95% CI 0.19-0.20)], start a university degree [aOR = 0.47 (95% CI 0.45-0.49)], obtain a university degree [aOR = 0.35 (95% CI 0.33-0.37)], and finish postgraduate education [aOR = 0.58 (95% CI 0.43-0.80)]. Results were attenuated but remained statistically significant in adjusted sibling comparison models. When psychiatric comorbidities were taken into account, the results were largely unchanged.

    CONCLUSIONS: Treatment-seeking individuals with SAD have substantially impaired academic performance throughout the formative years. Early detection and intervention are warranted to minimise the long-term socioeconomic impact of the disorder.

  • 33.
    Virtanen, Suvi
    et al.
    Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, Ralf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Mataix-Cols, David
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Centre for Psychiatry Research, Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Jayaram-Lindström, Nitya
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Centre for Psychiatry Research, Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, USA.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Rück, Christian
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Centre for Psychiatry Research, Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Suvisaari, Jaana
    National Institute for Health and Welfare, Helsinki, Finland.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Latvala, Antti
    Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Comorbidity of substance misuse with anxiety-related and depressive disorders: a genetically informative population study of 3 million individuals in Sweden2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, p. 1-10Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Causes of the comorbidity of substance misuse with anxiety-related and depressive disorders (anxiety/depression) remain poorly known. We estimated associations of substance misuse and anxiety/depression in the general population and tested them while accounting for genetic and shared environmental factors.

    METHODS: We studied individuals born in Sweden 1968-1997 (n = 2 996 398) with follow-up in nationwide register data for 1997-2013. To account for familial effects, stratified analyses were conducted within siblings and twin pairs. Substance misuse was defined as ICD-10 alcohol or drug use disorder or an alcohol/drug-related criminal conviction. Three dimensions of ICD-10 anxiety and depressive disorders and a substance misuse dimension were identified through exploratory factor analysis.

    RESULTS: Substance misuse was associated with a 4.5-fold (95% CI 4.50-4.58) elevated risk of lifetime generalized anxiety/depression, 4.7-fold (95% CI 4.63-4.82) elevated risk of panic disorder and agora/social phobia, and 2.9-fold elevated risk of phobias/OCD (95% CI 2.82-3.02) as compared to those without substance misuse. The associations were attenuated in within-family analyses but we found elevated risks in monozygotic twin pairs discordant for substance misuse as well as significant non-shared environmental correlations. The association between anxiety/depression and substance misuse was mainly driven by generalized anxiety/depression, whereas other anxiety/depression dimensions had minor or no independent associations with substance misuse.

    CONCLUSIONS: Substance misuse and anxiety/depression are associated at the population level, and these associations are partially explained by familial liabilities. Our findings indicate a common genetic etiology but are also compatible with a potential partially causal relationship between substance misuse and anxiety/depression.

  • 34.
    Yao, Shuyang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Norring, Claes
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Karolinska Institutet, & Stockholm Health Care Services, Stockholm County Council, Sweden.
    Birgegård, Andreas
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Karolinska Institutet, & Stockholm Health Care Services, Stockholm County Council, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    DʼOnofrio, Brian M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Thornton, Laura M.
    Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
    Bulik, Cynthia M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
    Kuja-Halkola, Ralf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Genetic and environmental contributions to diagnostic fluctuation in anorexia nervosa and bulimia nervosa2019In: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Anorexia nervosa and bulimia nervosa are two severe eating disorders associated with high premature mortality, suicidal risk and serious medical complications. Transition between anorexia nervosa and bulimia nervosa over the illness course and familial co-aggregation of the two eating disorders imply aetiological overlap. However, genetic and environmental liabilities to the overlap are poorly understood. Quantitative genetic research using clinical diagnosis is needed.

    METHODS: We acquired a clinical diagnosis of anorexia nervosa (prevalence = 0.90%) and bulimia nervosa (prevalence = 0.48%) in a large population-based sample (N = 782 938) of randomly selected full-sisters and maternal half-sisters born in Sweden between 1970 and 2005. Structural equation modelling was applied to quantify heritability of clinically diagnosed anorexia nervosa and bulimia nervosa and the contributions of genetic and environmental effects on their overlap.

    RESULTS: The heritability of clinically diagnosed anorexia nervosa and bulimia nervosa was estimated at 43% [95% confidence interval (CI) (36-50%)] and 41% (31-52%), respectively, in the study population, with the remaining variance explained by variance in unique environmental effects. We found statistically significant genetic [0.66, 95% CI (0.49-0.82)] and unique environmental correlations [0.55 (0.43-0.66)] between the two clinically diagnosed eating disorders; and their overlap was about equally explained by genetic and unique environmental effects [co-heritability 47% (35-58%)].

    CONCLUSIONS: Our study supports shared mechanisms for anorexia nervosa and bulimia nervosa and extends the literature from self-reported behavioural measures to clinical diagnosis. The findings encourage future molecular genetic research on both eating disorders and emphasize clinical vigilance for symptom fluctuation between them.

1 - 34 of 34
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