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  • 1.
    Alaie, Iman
    et al.
    Dept Psychol, Uppsala Univ, Uppsala, Sweden.
    Frick, Andreas
    Dept Psychol, Uppsala Univ, Uppsala, Sweden.
    Marteinsdottir, Ina
    Dept Clin & Expt Med, Linköping Univ, Linköping, Sweden.
    Hartvig, Per
    Dept Drug Design & Pharmacol, Univ Copenhagen, Copenhagen, Denmark.
    Tillfors, Maria
    Örebro University, School of Law, Psychology and Social Work.
    Eriksson, Elias
    Dept Pharmacol, Univ Gothenburg, Gothenburg, Sweden.
    Fredrikson, Mats
    Dept Psychol, Uppsala Univ, Uppsala, Sweden.
    Furmark, Tomas
    Dept Psychol, Uppsala Univ, Uppsala, Sweden.
    Serotonin Synthesis Rate and the Tryptophan Hydroxylase-2 G-703T Polymorphism in Social Anxiety Disorder2014In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 75, no 9, p. 357S-357SArticle in journal (Other academic)
  • 2.
    Brander, Gustaf
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, Ralf
    Karolinska Institutet, Stockholm, Sweden.
    Rosenqvist, Mina
    Karolinska Institutet, Stockholm, Sweden.
    Rück, Christian
    Karolinska Institutet, Stockholm, Sweden.
    Serlachius, Eva
    Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences.
    Mataix-Cols, David
    Karolinska Institutet, Stockholm, Sweden.
    Is Tic-Related OCD a Familial Subtype of the Disorder?: A Swedish Population Cohort Study2019In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 85, no 10, p. S221-S221Article in journal (Other academic)
  • 3.
    Brikell, Isabell
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ghirardi, Laura
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 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, United States.
    Dunn, David W.
    Department of Psychiatry, Riley Child and Adolescent Psychiatry Clinic, Indiana University School of Medicine, Indiana University Health Physicians, Indianapolis Indiana, United States.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Dalsgaard, Søren
    National Centre for Register-Based Research, Department of Economics, Aarhus University, Aarhus, Denmark; The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus University, Aarhus, Denmark; Department for Child and Adolescent Psychiatry, Hospital of Telemark, Kragerø, Norway.
    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.
    Familial Liability to Epilepsy and Attention-Deficit/Hyperactivity Disorder: A Nationwide Cohort Study2018In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 83, no 2, p. 173-180Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Epilepsy and attention-deficit/hyperactivity disorder (ADHD) are strongly associated; however, the underlying factors contributing to their co-occurrence remain unclear. A shared genetic liability has been proposed as one possible mechanism. Therefore, our goal in this study was to investigate the familial coaggregation of epilepsy and ADHD and to estimate the contribution of genetic and environmental risk factors to their co-occurrence.

    METHODS: We identified 1,899,654 individuals born between 1987 and 2006 via national Swedish registers and linked each individual to his or her biological relatives. We used logistic regression to estimate the association between epilepsy and ADHD within individual and across relatives. Quantitative genetic modeling was used to decompose the cross-disorder covariance into genetic and environmental factors.

    RESULTS: Individuals with epilepsy had a statistically significant increased risk of ADHD (odds ratio [OR] = 3.47, 95% confidence interval [CI] = 3.33-3.62). This risk increase extended to children whose mothers had epilepsy (OR = 1.85, 95% CI = 1.75-1.96), children whose fathers had epilepsy (OR = 1.64, 95% CI = 1.54-1.74), full siblings (OR = 1.56, 95% CI = 1.46-1.67), maternal half siblings (OR = 1.28, 95% CI = 1.14-1.43), paternal half siblings (OR = 1.10, 95% CI = 0.96-1.25), and cousins (OR = 1.15, 95% CI = 1.10-1.20). The genetic correlation was 0.21 (95% CI = 0.02-0.40) and explained 40% of the phenotypic correlation between epilepsy and ADHD, with the remaining variance largely explained by nonshared environmental factors (49%, nonshared environmental correlation = 0.36, 95% CI = 0.23-0.49). The contribution of shared environmental factors to the cross-disorder overlap was not statistically significant (11%, shared environmental correlation = 0.32, 95% CI = 20.16-0.79).

    CONCLUSIONS: This study demonstrates a strong and etiologically complex association between epilepsy and ADHD, with shared familial factors and risk factors unique to the individual contributing to co-occurrence of the disorders. Our findings suggest that epilepsy and ADHD may share less genetic risk as compared with other neurodevelopmental disorders.

  • 4.
    Chang, Zheng
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Quinn, Patrick D.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Lichtenstein, Paul
    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.
    Medication for Attention-Deficit/Hyperactivity Disorder and Risk for Depression: A Nationwide Longitudinal Cohort Study2016In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 80, no 12, p. 916-922Article in journal (Refereed)
    Abstract [en]

    Background: Attention-deficit/hyperactivity disorder (ADHD) is associated with high rates of psychiatric comorbidity, including depression. However, it is unclear whether ADHD medication increases or decreases the risk for depression.

    Methods: We studied all individuals with a diagnosis of ADHD born between 1960 and 1998 in Sweden (N = 38,752). We obtained data for prescription of ADHD medication, diagnosis of depression and other psychiatric disorders, and sociodemographic factors from population-based registers. The association between ADHD medication and depression was estimated with Cox proportional hazards regression.

    Results: After adjustment for sociodemographic and clinical confounders, ADHD medication was associated with a reduced long-term risk (i.e., 3 years later) for depression (hazard ratio = 0.58; 95% confidence interval, 0.51-0.67). The risk was lower for longer duration of ADHD medication. Also, ADHD medication was associated with reduced rates of concurrent depression; within-individual analysis suggested that occurrence of depression was 20% less common during periods when patients received ADHD medication compared with periods when they did not (hazard ratio = 0.80; 95% confidence interval, 0.70-0.92).

    Conclusions Our study suggests that ADHD medication does not increase the risk of later depression; rather, medication was associated with a reduced risk for subsequent and concurrent depression.

  • 5.
    Chang, Zheng
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ghirardi, Laura
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Quinn, Patrick D.
    Department of Applied Health Science, School of Public Health, Bloomington Indiana, USA.
    Asherson, Philip
    Social Genetic and Developmental Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, United Kingdom.
    D'Onofrio, Brian M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychological and Brain Sciences, Indiana University, Bloomington Indiana, USA.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Risks and Benefits of Attention-Deficit/Hyperactivity Disorder Medication on Behavioral and Neuropsychiatric Outcomes: A Qualitative Review of Pharmacoepidemiology Studies Using Linked Prescription Databases2019In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 86, no 5, p. 335-343Article, review/survey (Refereed)
    Abstract [en]

    Attention-deficit/hyperactivity disorder (ADHD) medication is one of the most commonly prescribed medication classes in child and adolescent psychiatry, and its use is increasing rapidly in adult psychiatry. However, major questions and concerns remain regarding the benefits and risks of ADHD medication, especially in real-world settings. We conducted a qualitative systematic review of studies that investigated the effects of ADHD medication on behavioral and neuropsychiatric outcomes using linked prescription databases from the last 10 years and identified 40 studies from Europe, North America, and Asia. Among them, 18 used within-individual designs to account for confounding by indication. These studies suggested short-term beneficial effects of ADHD medication on several behavioral or neuropsychiatric outcomes (i.e., injuries, motor vehicle accidents, education, substance use disorder), with estimates suggesting relative risk reduction of 9% to 58% for these outcomes. The within-individual studies found no evidence of increased risks for suicidality and seizures. Replication studies are needed for several other important outcomes (i.e., criminality, depression, mania, psychosis). The available evidence from pharmacoepidemiology studies on long-term effects of ADHD medication was less clear. We discuss time-varying confounding and other limitations that should be considered when interpreting results from pharmacoepidemiology studies. Furthermore, we highlight several knowledge gaps to be addressed in future research and implications for research on mechanisms of outcomes of ADHD medications.

  • 6.
    Faraone, Stephen
    et al.
    SUNY Upstate Medical University, Syracuse NY, USA.
    James, Yanli Zhang
    SUNY Upstate Medical University, Syracuse NY, USA.
    Chen, Qi
    Örebro University, Örebro, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences.
    Predicting Comorbid Disorders in ADHD Using Machine Learning2019In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 85, no 10, p. S6-S6Article in journal (Other academic)
  • 7.
    Fernández de la Cruz, Lorena
    et al.
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden.
    Rydell, Mina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Runeson, Bo
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Brander, Gustaf
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden.
    Rück, Christian
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden.
    D'Onofrio, Brian M
    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.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Mataix-Cols, David
    Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Suicide in Tourette's and Chronic Tic Disorders2017In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 82, no 2, p. 111-118Article in journal (Refereed)
    Abstract [en]

    Background: Persons with neuropsychiatric disorders are at increased risk of suicide, but there is little data concerning Tourette's and chronic tic disorders (TD/CTD). We aimed to quantify the risk of suicidal behavior in a large nationwide cohort of patients with TD/CTD, establish the contribution of psychiatric comorbidity to this risk, and identify predictors of suicide.

    Methods: Using a validated algorithm, we identified 7736 TD/CTD cases in the Swedish National Patient Register during a 44-year period (1969-2013). Using a matched case-cohort design, patients were compared with general population control subjects (1:10 ratio). Risk of suicidal behavior was estimated using conditional logistic regressions. Predictors of suicidal behavior in the TD/CTD cohort were studied using Cox regression models.

    Results: In unadjusted models, TD/CTD patients, compared with control subjects, had an increased risk of both dying by suicide (odds ratio: 4.39; 95% confidence interval [CI]: 2.89-6.67) and attempting suicide (odds ratio: 3.86; 95% CI: 3.50-4.26). After adjusting for psychiatric comorbidities, the risk was reduced but remained substantial. Persistence of tics beyond young adulthood and a previous suicide attempt were the strongest predictors of death by suicide in TD/CTD patients (hazard ratio: 11.39; 95% CI: 3.71-35.02, and hazard ratio: 5.65; 95% CI: 2.21-14.42, respectively).

    Conclusions: TD/CTD are associated with substantial risk of suicide. Suicidal behavior should be monitored in these patients, particularly in those with persistent tics, history of suicide attempts, and psychiatric comorbidities. Preventive and intervention strategies aimed to reduce the suicidal risk in this group are warranted.

  • 8.
    Humble, Mats B.
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Uppsala university.
    Bejerot, Susanne
    Uppsala university.
    Bergqvist, Peter B. F.
    AstraZeneca, Lund, Sweden.
    Reactivity of serotonin in whole blood: response to Mulder et al.2002In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 51, no 3, p. 267-268Article in journal (Other academic)
  • 9.
    Humble, Mats
    et al.
    Psychiatry of Northern Dalecarlia, Mora Hospital, Mora, Sweden; Karolinska Institutet, Division of Psychiatry, Danderyd Hospital, Danderyd, Sweden.
    Bejerot, Susanne
    Department of Neuroscience, Division of Psychiatry, Uppsala University, Uppsala, Sweden.
    Bergqvist, P. B.
    Department of Clinical Pharmacology, Lund University, Lund, Sweden.
    Bengtsson, F.
    Department of Clinical Pharmacology, Lund University, Lund Sweden; Department of Neuroscience and Locomotion, Division of Psychiatry, Linköping University Hospital, Linköping, Sweden.
    Reactivity of serotonin in whole blood: relationship with drug response in obsessive-compulsive disorder2001In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 49, no 4, p. 360-368Article in journal (Refereed)
    Abstract [en]

    Background: Obsessive-compulsive disorder responds almost only to potent serotonin reuptake inhibitors. Previous studies have suggested a relation between serotonergic function and clinical outcome in serotonin reuptake inhibitor treatment of obsessive-compulsive disorder.

    Methods: In a randomized, double-blind trial, comparing clomipramine, paroxetine, and a placebo in obsessive-compulsive disorder, serotonin levels in whole blood (WB-5-HT) were measured at baseline, after 1 week, and after 4 weeks of treatment and related to clinical outcome in 36 patients.

    Results: In patients treated with serotonin reuptake inhibitors there was a pronounced decrease of WB-5-HT, variable after 1 week and uniformly maximal after 4 weeks. The decrease of WB-5-HT after 1 week of serotonin reuptake inhibitor treatment correlated negatively with clinical outcome after 12 weeks (r = -.61, p =.0006); hence, patients with slower WB-5-HT reactivity eventually responded better to treatment. Baseline WB-5-HT, but not WB-5-HT reactivity, was related to season. Depression, autistic traits, and previous serotonin reuptake inhibitor treatment predicted nonresponse.

    Conclusions: A fast decrease of WB-5-HT was associated with poor clinical outcome. This may be related to faster serotonin efflux from platelets, which has previously been linked to autism. Further studies are necessary to identify the underlying mechanism and discern whether serotonin reuptake inhibitor-induced WB-5-HT decrease is clinically useful.

  • 10.
    Isomura, Kayoko
    et al.
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Brander, Gustaf
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Chang, Zheng
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, Ralf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Rück, Christian
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Hellner, Clara
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Lichtenstein, Paul
    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
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    de la Cruz, Lorena Fernandez
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Metabolic and Cardiovascular Complications in Obsessive-Compulsive Disorder: A Total Population, Sibling Comparison Study With Long-Term Follow-up2018In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 84, no 5, p. 324-331Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Obsessive-compulsive disorder (OCD) is associated with increased mortality, but the causes of this increase are poorly understood. This study examined whether OCD is associated with an increased risk of metabolic and cardiovascular complications.

    METHODS: Individuals diagnosed with OCD (n = 25,415) were identified from a cohort of 12,497,002 individuals living in Sweden between 1973 and 2013. Cox proportional hazard regression analyses were used to investigate the risk of metabolic and cardiovascular complications in OCD patients compared with the general population and unaffected full siblings of OCD individuals. Exploratory analyses were used to examine the effect of treatment with serotonin reuptake inhibitors, with or without antipsychotics, on the outcomes of interest.

    RESULTS: Individuals with OCD had a higher risk of any metabolic or cardiovascular complications compared with the general population (adjusted hazard ratio = 1.45; 95% confidence interval = 1.42-1.49) and their unaffected full siblings (adjusted hazard ratio = 1.47; 95% confidence interval = 1.40-1.54). In the fully adjusted sibling comparison models, patients had higher risks of obesity, type 2 diabetes mellitus, and circulatory system diseases. The risks were already evident from the beginning of the follow-up period and remained largely unchanged when excluding different groups of psychiatric comorbidities. Compared with patients who were not taking serotonin reuptake inhibitors, patients taking higher doses of serotonin reuptake inhibitors and who had a longer duration of treatment had significantly lower risks of metabolic and cardiovascular complications, regardless of whether they were also taking antipsychotics.

    CONCLUSIONS: OCD is associated with an increased risk of metabolic and cardiovascular complications. Our results underscore the importance of carefully monitoring metabolic and cardiovascular health in patients with OCD early in the course of the disorder.

  • 11.
    Madrid-Gambin, Francisco
    et al.
    Department of Psychiatry, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
    Focking, Melanie
    Department of Psychiatry, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
    Sabherwal, Sophie
    Department of Psychiatry, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
    Heurich, Meike
    School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Cardiff, United Kingdom.
    English, Jane A.
    Department of Psychiatry, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
    O'Gorman, Aoife
    Institute of Food and Health, UCD School of Agriculture and Food Science, Dublin, Ireland.
    Suvitaival, Tommi
    Steno Diabetes Center Copenhagen, Gentofte, Denmark.
    Ahonen, Linda
    Steno Diabetes Center Copenhagen, Gentofte, Denmark.
    Cannon, Mary
    Department of Psychiatry, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
    Lewis, Glyn
    Faculty of Brain Sciences, Division of Psychiatry, University College London, London, United Kingdom.
    Mattila, Ismo
    Steno Diabetes Center Copenhagen, Gentofte, Denmark.
    Scaife, Caitriona
    Department of Psychiatry, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
    Madden, Sean
    Department of Psychiatry, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
    Hyötyläinen, Tuulia
    Örebro University, School of Science and Technology. Department of Chemistry.
    Oresic, Matej
    Örebro University, School of Medical Sciences. Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
    Zammit, Stanley
    MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom; Centre for Academic Mental Health, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
    Cagney, Gerard
    Conway Institute, UCD School of Biomolecular and Biomedical Science, University College Dublin, Dublin, Ireland.
    Cotter, David R.
    Department of Psychiatry, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
    Brennan, Lorraine
    Institute of Food and Health, UCD School of Agriculture and Food Science, Dublin, Ireland.
    Integrated Lipidomics and Proteomics Point to Early Blood-Based Changes in Childhood Preceding Later Development of Psychotic Experiences: Evidence From the Avon Longitudinal Study of Parents and Children2019In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 86, no 1, p. 25-34Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The identification of early biomarkers of psychotic experiences (PEs) is of interest because early diagnosis and treatment of those at risk of future disorder is associated with improved outcomes. The current study investigated early lipidomic and coagulation pathway protein signatures of later PEs in subjects from the Avon Longitudinal Study of Parents and Children cohort.

    METHODS: Plasma of 115 children (12 years of age) who were first identified as experiencing PEs at 18 years of age (48 cases and 67 controls) were assessed through integrated and targeted lipidomics and semitargeted proteomics approaches. We assessed the lipids, lysophosphatidylcholines (n = 11) and phosphatidylcholines (n = 61), and the protein members of the coagulation pathway (n = 22) and integrated these data with complement pathway protein data already available on these subjects.

    RESULTS: Twelve phosphatidylcholines, four lysophosphatidylcholines, and the coagulation protein plasminogen were altered between the control and PEs groups after correction for multiple comparisons. Lipidomic and proteomic datasets were integrated into a multivariate network displaying a strong relationship between most lipids that were significantly associated with PEs and plasminogen. Finally, an unsupervised clustering approach identified four different clusters, with one of the clusters presenting the highest case-control ratio (p < .01) and associated with a higher concentration of smaller low-density lipoprotein cholesterol particles.

    CONCLUSIONS: Our findings indicate that the lipidome and proteome of subjects who report PEs at 18 years of age are already altered at 12 years of age, indicating that metabolic dysregulation may contribute to an early vulnerability to PEs and suggesting crosstalk between these lysophosphatidylcholines, phosphatidylcholines, and coagulation and complement proteins.

  • 12.
    Martin, Joanna
    et al.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden; Stanley Center for Psychiatric Research, Broad Institute, Cambridge Massachusetts, United States; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston Massachusetts, United States; MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom.
    Walters, Raymond K.
    Stanley Center for Psychiatric Research, Broad Institute, Cambridge Massachusetts, United States; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston Massachusetts, United States.
    Demontis, Ditte
    Centre for Integrative Sequencing [iSEQ], Aarhus University, Aarhus, Roskilde, Denmark; Department of Biomedicine–Human Genetics, Aarhus University, Aarhus, Roskilde, Denmark.
    Mattheisen, Manuel
    Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden; Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; Centre for Integrative Sequencing [iSEQ], Aarhus University, Aarhus, Roskilde, Denmark; Department of Biomedicine–Human Genetics, Aarhus University, Aarhus, Roskilde, Denmark.
    Lee, S. Hong
    Queensland Brain Institute, University of Queensland, Brisbane Queensland, Australia; School of Environmental and Rural Science, University of New England, Armidale NSW, Australia; Centre for Population Health Research, School of Health Sciences and Sansom Institute of Health Research, University of South Australia, Adelaide, Australia.
    Robinson, Elise
    Stanley Center for Psychiatric Research, Broad Institute, Cambridge Massachusetts, United States; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston Massachusetts, United States.
    Brikell, Isabell
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ghirardi, Laura
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Eriksson, Nicholas
    23andMe Inc., Mountain View California, United States.
    Werge, Thomas
    Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; Institute of Biological Psychiatry, MHC Sct. Hans, Mental Health Services Copenhagen, Roskilde, Denmark; Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
    Mortensen, Preben Bo
    Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; Centre for Integrative Sequencing [iSEQ], Aarhus University, Aarhus, Roskilde, Denmark; National Centre for Register-Based Research, Aarhus University, Aarhus, Roskilde, Denmark; Centre for Integrated Register-Based Research, Aarhus University, Aarhus, Roskilde, Denmark.
    Pedersen, Marianne Giortz
    Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; National Centre for Register-Based Research, Aarhus University, Aarhus, Roskilde, Denmark; Centre for Integrated Register-Based Research, Aarhus University, Aarhus, Roskilde, Denmark.
    Mors, Ole
    Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; Psychosis Research Unit, Aarhus University Hospital, Risskov, Denmark.
    Nordentoft, Merete
    Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; Mental Health Services in the Capital Region of Denmark, Mental Health Center Copenhagen, University of Copenhagen, Copenhagen, Denmark.
    Hougaard, David M.
    Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; Center for Neonatal Screening, Department for Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark.
    Bybjerg-Grauholm, Jonas
    Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; Center for Neonatal Screening, Department for Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark.
    Wray, Naomi R.
    Queensland Brain Institute, University of Queensland, Brisbane Queensland, Australia.
    Franke, Barbara
    Departments of Human Genetics and Psychiatry, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, Netherlands.
    Faraone, Stephen V.
    Departments of Psychiatry and of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse NY, United States; K.G. Jebsen Centre for Research on Neuropsychiatric Disorders, University of Bergen, Bergen, Norway.
    O'Donovan, Michael C.
    MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom.
    Thapar, Anita
    MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom.
    Børglum, Anders D.
    Lundbeck Foundation Initiative for Integrative Psychiatric Research [iPSYCH], Aarhus, Roskilde, Denmark; Centre for Integrative Sequencing [iSEQ], Aarhus University, Aarhus, Roskilde, Denmark; Department of Biomedicine–Human Genetics, Aarhus University, Aarhus, Roskilde, Denmark.
    Neale, Benjamin M.
    Stanley Center for Psychiatric Research, Broad Institute, Cambridge Massachusetts, United States; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston Massachusetts, United States.
    A Genetic Investigation of Sex Bias in the Prevalence of Attention-Deficit/Hyperactivity Disorder2018In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 83, no 12, p. 1044-1053Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) shows substantial heritability and is two to seven times more common in male individuals than in female individuals. We examined two putative genetic mechanisms underlying this sex bias: sex-specific heterogeneity and higher burden of risk in female cases.

    METHODS: We analyzed genome-wide autosomal common variants from the Psychiatric Genomics Consortium and iPSYCH Project (n = 20,183 cases, n = 35,191 controls) and Swedish population register data (n = 77,905 cases, n = 1,874,637 population controls).

    RESULTS: Genetic correlation analyses using two methods suggested near complete sharing of common variant effects across sexes, with r(g) estimates close to 1. Analyses of population data, however, indicated that female individuals with ADHD may be at especially high risk for certain comorbid developmental conditions (i.e., autism spectrum disorder and congenital malformations), potentially indicating some clinical and etiological heterogeneity. Polygenic risk score analysis did not support a higher burden of ADHD common risk variants in female cases (odds ratio [confidence interval] = 1.02 [0.98-1.06], p = .28). In contrast, epidemiological sibling analyses revealed that the siblings of female individuals with ADHD are at higher familial risk for ADHD than the siblings of affected male individuals (odds ratio [confidence interval] = 1.14 [1.11-1.18], p = 1.5E-15).

    CONCLUSIONS: Overall, this study supports a greater familial burden of risk in female individuals with ADHD and some clinical and etiological heterogeneity, based on epidemiological analyses. However, molecular genetic analyses suggest that autosomal common variants largely do not explain the sex bias in ADHD prevalence.

  • 13.
    Skoglund, Charlotte
    et al.
    Departments of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Chen, Qi
    Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Franck, Johan
    Departments of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Attention-deficit/hyperactivity disorder and risk for substance use disorders in relatives2015In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 77, no 10, p. 880-886Article in journal (Refereed)
    Abstract [en]

    Background: Previous research indicates that attention-deficit/hyperactivity disorder (ADHD) is highly associated with substance use disorders (SUD). However, these studies have failed to clarify the nature of the overlap. The main aim of this study was to explore whether the overlap between ADHD and SUD could be explained by shared genetic and environmental factors or by harmful effects of ADHD medication.

    Methods: We employed a matched cohort design across different levels of family relatedness recorded from 1973-2009. By linking longitudinal Swedish national registers, 62,015 ADHD probands and first-degree and second-degree relatives were identified and matched 1:10 with control subjects without ADHD and their corresponding relatives. Any record of SUD was defined by discharge diagnoses of the International Classification of Diseases or a purchase of any drug used in the treatment of SUD.

    Results: First-degree relatives of ADHD probands were at elevated risk for SUD (odds ratios 2.2 and 1.8) compared with relatives of control subjects. The corresponding relative risk in second-degree relatives was substantially lower (odd ratios 1.4 and 1.4). The familial aggregation patterns remained similar for first-degree and second-degree relatives after excluding individuals with coexisting disorders such as schizophrenia, bipolar disorder, depression, and conduct disorder.

    Conclusions: Our findings suggest that the co-occurrence of ADHD and SUD is due to genetic factors shared between the two disorders, rather than to a general propensity for psychiatric disorders or harmful effects of ADHD medication.

  • 14.
    Song, Jie
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Kuja-Halkola, Ralf
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bergen, Sarah E.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Stanley Center for Psychiatric Research, the Broad Institute of MIT and Harvard, Cambridge Massachusetts, USA.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Landén, Mikael
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Institute of Neuroscience and Physiology, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Specificity in Etiology of Subtypes of Bipolar Disorder: Evidence From a Swedish Population-Based Family Study2018In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 84, no 11, p. 810-816Article in journal (Refereed)
    Abstract [en]

    Background: Uncertainty remains whether bipolar I disorder (BDI) and bipolar II disorder (BDII) differ etiologically. We used a population-based family sample to examine the etiological boundaries between BDI and BDII by assessing their familial aggregation/coaggregation and by assessing the coaggregation between them and schizophrenia, depression, attention-deficit/hyperactivity disorder, eating disorders, autism spectrum disorder, substance use disorders, anxiety disorders, and personality disorders.

    Methods: By linking Swedish national registers, we established a population-based cohort (N = 15,685,511) and identified relatives with different biological relationships. Odds ratios (ORs) were used to measure the relative risk of BDI and BDII in relatives of individuals diagnosed with BDI (n = 4309) and BDII (n = 4178). The heritability for BDI and BDII and the genetic correlation across psychiatric disorders were estimated by variance decomposition analysis.

    Results: Compared with the general population, the OR of BDI was 17.0 (95% confidence interval [CI] 13.1-22.0) in first-degree relatives of BDI patients, higher than that of BDII patients (OR 9.8, 95% CI 7.7-12.5). The ORs of BDII were 13.6 (95% CI 10.2-18.2) in first-degree relatives of BDII patients and 9.8 (95% CI 7.7-12.4) in relatives of BDI patients. The heritabilities for BDI and BDII were estimated at 57% (95% CI 32%-79%) and 46% (95% CI 21%-67%), respectively, with a genetic correlation estimated as 0.78 (95% CI 0.36-1.00). The familial coaggregation of other psychiatric disorders, in particular schizophrenia, showed different patterns for BDI and BDII.

    Conclusions: Our results suggest a distinction between BDI and BDII in etiology, partly due to genetic differences.

  • 15.
    Walum, Hasse
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Neiderhiser, Jenae M.
    Department of Psychology, Pennsylvania State University, Philadelphia PA, United States .
    Reiss, David
    Yale Child Study Center, Yale University, New Haven CT, United States.
    Ganiban, Jody M.
    Department of Psychology, George Washington University, Washington DC, United States .
    Spotts, Erica L.
    Division of Behavioral and Social Research, National Institute on Aging, Bethesda MD, United States.
    Pedersen, Nancy L.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Anckarsäter, Henrik
    Department of Psychiatry and Neurochemistry, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden .
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Westberg, Lars
    Department of Pharmacology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Variation in the oxytocin receptor gene is associated with pair-bonding and social behavior2012In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 71, no 5, p. 419-426Article in journal (Refereed)
    Abstract [en]

    Background: In specific vole and primate species the neuropeptide oxytocin plays a central role in the regulation of pair-bonding behavior. Here we investigate the extent to which genetic variants in the oxytocin receptor gene (OXTR) are associated with pair-bonding and related social behaviors in humans.

    Methods: We first genotyped twelve single nucleotide polymorphisms (SNPs) in the TOSS (Twin and Offspring Study in Sweden) (n = 2309) and the TCHAD (Swedish Twin Study of Child and Adolescent Development) (n = 1240), comprising measures of self-reported pair-bonding behavior. In the TOSS sample we further investigated one of the SNPs for measures of marital status and quality. Moreover, in the TCHAD sample we explored the longitudinal relationship between precursors of pair-bonding during childhood and subsequent behavior in romantic relationships. Finally, in the TCHAD study and in the Child and Adolescent Twin Study of Sweden (CATSS) (n = 1771), the association between the same SNP and childhood behaviors was investigated.

    Results: One SNP (rs7632287) in OXTR was associated with traits reflecting pair-bonding in women in the TOSS and TCHAD samples. In girls the rs7632287 SNP was further associated with childhood social problems, which longitudinally predicted pair-bonding behavior in the TCHAD sample. This association was replicated in the CATSS sample in which an association between the same SNP and social interaction deficit symptoms from the autism spectrum was detected.

    Conclusion: These results suggest an association between variation in OXTR and human pair-bonding and other social behaviors, possibly indicating that the well-described influence of oxytocin on affiliative behavior in voles could also be of importance for humans.

  • 16.
    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.
    Bergen, Andrew
    Berrettini, Wade
    Boni, Claudette
    Perica, Vesna Boraska
    Brandt, Harry
    Burghardt, Roland
    Cassina, Matteo
    Cesta, Carolyn
    Clementi, Maurizio
    Coleman, Joni
    Cone, Roger
    Courtet, Philippe
    Crawford, Steven
    Crow, Scott
    Crowley, James
    Danner, Unna
    Davis, Oliver
    de Zwaan, Martina
    Dedoussis, George
    Degortes, Daniela
    DeSocio, Janiece
    Dick, Danielle
    Dikeos, Dimitris
    Dmitrzak-Weglarz, Monika
    Docampo, Elisa
    Egberts, Karin
    Ehrlich, Stefan
    Escaramis, Georgia
    Esko, Tonu
    Estivill, Xavier
    Favaro, Angela
    Fernandez-Aranda, Fernando
    Fichter, Manfred
    Finan, Chris
    Fischer, Krista
    Focker, Manuel
    Foretova, Lenka
    Forzan, Monica
    Franklin, Christopher
    Gaspar, Helena
    Gonidakis, Fragiskos
    Gorwood, Philip
    Gratacos, Monica
    Guillaume, Sebastien
    Guo, Yiran
    Hakonarson, Hakon
    Halmi, Katherine
    Hatzikotoulas, Konstantinos
    Hauser, Joanna
    Hebebrand, Johannes
    Helder, Sietske
    Hendriks, Judith
    Herpertz-Dahlmann, Beate
    Herzog, Wolfgang
    Hilliard, Christopher
    Hinney, Anke
    Huckins, Laura
    Hudson, James
    Huemer, Julia
    Imgart, Hartmut
    Inoko, Hidetoshi
    Jimenez-Murcia, Susana
    Johnson, Craig
    Jordan, Jenny
    Jureus, Anders
    Kalsi, Gursharan
    Kaminska, Debora
    Kaplan, Allan
    Kaprio, Jaakko
    Karhunen, Leila
    Karwautz, Andreas
    Kas, Martien
    Kaye, Walter
    Kennedy, James
    Kennedy, Martin
    Keski-Rahkonen, Anna
    Kiezebrink, Kirsty
    Kim, Youl-Ri
    Klump, Kelly
    Knudsen, Gun Peggy
    Koeleman, Bobby
    Koubek, Doris
    La Via, Maria
    Landen, Mikael
    Levitan, Robert
    Li, Dong
    Lilenfeld, Lisa
    Lissowska, Jolanta
    Magistretti, Pierre
    Maj, Mario
    Mannik, Katrin
    Martin, Nicholas
    McDevitt, Sara
    McGuffin, Peter
    Merl, Elisabeth
    Metspalu, Andres
    Meulenbelt, Ingrid
    Micali, Nadia
    Mitchell, James
    Mitchell, Karen
    Monteleone, Palmiero
    Monteleone, Alessio Maria
    Mortensen, Preben
    Munn-Chernoff, Melissa
    Nacmias, Benedetta
    Nilsson, Ida
    Ntalla, Ioanna
    O'Toole, Julie
    Pantel, Jacques
    Papezova, Hana
    Parker, Richard
    Rabionet, Raquel
    Raevuori, Anu
    Rajewski, Andrzej
    Ramoz, Nicolas
    Rayner, N. William
    Reichborn-Kjennerud, Ted
    Ricca, Valdo
    Ripke, Stephan
    Ritschel, Franziska
    Roberts, Marion
    Rotondo, Alessandro
    Rybakowski, Filip
    Santonastaso, Paolo
    Schmidt, Ulrike
    Schork, Nicholas
    Schosser, Alexandra
    Seitz, Jochen
    Slachtova, Lenka
    Slagboom, P. Eline
    Slof-Op't Landt, Margarita
    Slopien, Agnieszka
    Smith, Tosha
    Sorbi, Sandro
    Strengman, Eric
    Strober, Michael
    Sullivan, Patrick
    Szatkiewicz, Jin
    Szeszenia-Dabrowska, Neonila
    Tachmazidou, Ioanna
    Tenconi, Elena
    Thornton, Laura
    Tortorella, Alfonso
    Tozzi, Federica
    Treasure, Janet
    Tsitsika, Artemis
    Tziouvas, Konstantinos
    van Elburg, Annemarie
    van Furth, Eric
    Wade, Tracey
    Wagner, Gudrun
    Walton, Esther
    Woodside, D. Blake
    Zeggini, Elefthena
    Zerwas, Stephanie
    Zipfel, Stephan
    Alfredsson, Lars
    Andreassen, Ole
    Aschauer, Harald
    Barrett, Jeffrey
    Bencko, Vladimir
    Carlberg, Laura
    Cichon, Sven
    Cohen-Woods, Sarah
    Dina, Christian
    Ding, Bo
    Espeseth, Thomas
    Floyd, James
    Gallinger, Steven
    Gambaro, Giovanni
    Giegling, Ina
    Herms, Stefan
    Janout, Vladimir
    Julia, Antonio
    Klareskog, Lars
    Le Hellard, Stephanie
    Leboyer, Marion
    Lundervold, Asti
    Marsal, Sara
    Mattingsdal, Morten
    Navratilova, Marie
    Ophoff, Roel
    Palotie, Aamo
    Pinto, Dalila
    Ripatti, Samuli
    Rujescu, Dan
    Scherer, Stephen
    Scott, Laura
    Sladek, Robert
    Soranzo, Nicole
    Southam, Lorraine
    Steen, Vidar
    Wichmann, H-Erich
    Widen, Elisabeth
    Breen, Gerome
    Bulik, Cynthia
    Associations Between Attention-Deficit/Hyperactivity Disorder and Various Eating Disorders: A Swedish Nationwide Population Study Using Multiple Genetically Informative Approaches2019In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 86, no 8, p. 577-586Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Although attention-deficit/hyperactivity disorder (ADHD) and eating disorders (EDs) frequently cooccur, little is known about the shared etiology. In this study, we comprehensively investigated the genetic association between ADHD and various EDs, including anorexia nervosa (AN) and other EDs such as bulimia nervosa.

    METHODS: We applied different genetically informative designs to register-based information of a Swedish nationwide population (N = 3,550,118). We first examined the familial coaggregation of clinically diagnosed ADHD and EDs across multiple types of relatives. We then applied quantitative genetic modeling in full-sisters and maternal half-sisters to estimate the genetic correlations between ADHD and EDs. We further tested the associations between ADHD polygenic risk scores and ED symptoms, and between AN polygenic risk scores and ADHD symptoms, in a genotyped population-based sample (N = 13,472).

    RESULTS: Increased risk of all types of EDs was found in individuals with ADHD (any ED: odds ratio [OR] = 3.97, 95% confidence interval [CI] = 3.81, 4.14; AN: OR = 2.68, 95% CI = 2.15, 2.86; other EDs: OR = 4.66, 95% CI = 4.47, 4.87; bulimia nervosa: OR = 5.01, 95% CI = 4.63, 5.41) and their relatives compared with individuals without ADHD and their relatives. The magnitude of the associations decreased as the degree of relatedness decreased, suggesting shared familial liability between ADHD and EDs. Quantitative genetic models revealed stronger genetic correlation of ADHD with other EDs (.37, 95% CI = .31, .42) than with AN (.14, 95% CI = .05, .22). ADHD polygenic risk scores correlated positively with ED symptom measures overall and with the subscales Drive for Thinness and Body Dissatisfaction despite small effect sizes.

    CONCLUSIONS: We observed stronger genetic association with ADHD for non-AN EDs than for AN, highlighting specific genetic correlation beyond a general genetic factor across psychiatric disorders.

1 - 16 of 16
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