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  • 1.
    Brännström, Jon
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Lövheim, Hugo
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Gustafson, Yngve
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Nordström, Peter
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Association Between Antidepressant Drug Use and Hip Fracture in Older People Before and After Treatment Initiation2019Inngår i: JAMA psychiatry, ISSN 2168-6238, E-ISSN 2168-622X, Vol. 76, nr 2, s. 172-179Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    IMPORTANCE: Treatment with antidepressants has been associated with hip fracture. This association could restrict the treatment options, especially in older patients. OBJECTIVE: To investigate the association between antidepressant drug treatment and hip fracture starting 1 year before the initiation of treatment. DESIGN, SETTING, AND PARTICIPANTS: In this nationwide cohort study, 204 072 individuals in the Prescribed Drugs Register of Sweden's National Board of Health and Welfare aged 65 years or older who had a prescription of antidepressants filled between July 1, 2006, and December 31, 2011, were matched by birth year and sex to 1 control participant who was not prescribed antidepressants (for a total of 408 144 people in the register). Outcome data were collected from 1 year before to 1 year after the index date (date of prescription being filled). Data analysis was performed from July 1, 2005, to December 31, 2012. EXPOSURES: First filled prescription of an antidepressant drug. MAIN OUTCOMES AND MEASURES: Incident hip fractures occurring in the year before and year after initiation of antidepressant therapy were registered. Associations were investigated using multivariable conditional logistic regression models and flexible parametric models. RESULTS: Of the 408 144 people in the register who were included in the study, 257 486 (63.1%) were women, with a mean (SD) age of 80.1 (7.2) years. Antidepressant users sustained more than twice as many hip fractures than did nonusers in the year before and year after the initiation of therapy (2.8% vs 1.1% and 3.5% vs 1.3%, respectively, per actual incidence figures). In adjusted analyses, the odds ratios were highest for the associations between antidepressant use and hip fracture 16 to 30 days before the prescription was filled (odds ratio, 5.76; 95% CI, 4.73-7.01). In all separate analyses of age groups, of men and women, and of individual antidepressants, the highest odds ratios were seen 16 to 30 days before initiation of treatment, and no clear dose-response relationship was seen. CONCLUSIONS AND RELEVANCE: The present study found an association between antidepressant drug use and hip fracture before and after the initiation of therapy. This finding raises questions about the association that should be further investigated in treatment studies.

  • 2. Musliner, Katherine L.
    et al.
    Mortensen, Preben B.
    McGrath, John J.
    Suppli, Nis P.
    Hougaard, David M.
    Bybjerg-Grauholm, Jonas
    Bækvad-Hansen, Marie
    Andreassen, Ole
    Pedersen, Carsten B.
    Pedersen, Marianne G.
    Mors, Ole
    Nordentoft, Merete
    Børglum, Anders D.
    Werge, Thomas
    Agerbo, Esben
    Nordin Adolfsson, Annelie ()
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Association of Polygenic Liabilities for Major Depression, Bipolar Disorder, and Schizophrenia With Risk for Depression in the Danish Population2019Inngår i: JAMA psychiatry, ISSN 2168-6238, E-ISSN 2168-622X, Vol. 76, nr 5, s. 516-525Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Importance: Although the usefulness of polygenic risk scores as a measure of genetic liability for major depression (MD) has been established, their association with depression in the general population remains relatively unexplored.

    Objective: To evaluate whether polygenic risk scores for MD, bipolar disorder (BD), and schizophrenia (SZ) are associated with depression in the general population and explore whether these polygenic liabilities are associated with heterogeneity in terms of age at onset and severity at the initial depression diagnosis.

    Design, Setting, and Participants: Participants were drawn from the Danish iPSYCH2012 case-cohort study, a representative sample drawn from the population of Denmark born between May 1, 1981, and December 31, 2005. The hazard of depression was estimated using Cox regressions modified to accommodate the case-cohort design. Case-only analyses were conducted using linear and multinomial regressions. The data analysis was conducted from February 2017 to June 2018.

    Exposures: Polygenic risk scores for MD, BD, and SZ trained using the most recent genome-wide association study results from the Psychiatric Genomics Consortium.

    Main Outcomes and Measures: The main outcome was first depressive episode (International Statistical Classification of Diseases and Related Health Problems, Tenth Revision [ICD-10] code F32) treated in hospital-based psychiatric care. Severity at the initial diagnosis was measured using the ICD-10 code severity specifications (mild, moderate, severe without psychosis, and severe with psychosis) and treatment setting (inpatient, outpatient, and emergency).

    Results: Of 34 573 participants aged 10 to 31 years at censoring, 68% of those with depression were female compared with 48.9% of participants without depression. Each SD increase in polygenic liability for MD, BD, and SZ was associated with 30% (hazard ratio [HR], 1.30; 95% CI, 1.27-1.33), 5% (HR, 1.05; 95% CI, 1.02-1.07), and 12% (HR, 1.12; 95% CI, 1.09-1.15) increases in the hazard of depression, respectively. Among cases, a higher polygenic liability for BD was associated with earlier depression onset (β = -.07; SE = .02; P = .002).

    Conclusions and Relevance: Polygenic liability for MD is associated with first depression in the general population, which supports the idea that these scores tap into an underlying liability for developing the disorder. The fact that polygenic risk for BD and polygenic risk for SZ also were associated with depression is consistent with prior evidence that these disorders share some common genetic overlap. Variations in polygenic liability may contribute slightly to heterogeneity in clinical presentation, but these associations appear minimal.

  • 3. Sahlin, Hanna
    et al.
    Kuja-Halkola, Ralf
    Bjureberg, Johan
    Lichtenstein, Paul
    Molero, Yasmina
    Rydell, Mina
    Hedman, Erik
    Runeson, Bo
    Jokinen, Jussi
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri. Karolinska Inst, Dept Clin Neurosci, Ctr Psychiat Res, Stockholm, Sweden.
    Ljotsson, Brjann
    Hellner, Clara
    Association Between Deliberate Self-harm and Violent Criminality2017Inngår i: JAMA psychiatry, ISSN 2168-6238, E-ISSN 2168-622X, Vol. 74, nr 6, s. 615-621Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    IMPORTANCE Individuals who self-harm may have an increased risk of aggression toward others, but this association has been insufficiently investigated. More conclusive evidence may affect assessment, treatment interventions, and clinical guidelines. OBJECTIVE To investigate the association between nonfatal self-harm and violent crime. DESIGN, SETTING, AND PARTICIPANTS This population-based longitudinal cohort study, conducted from January 1, 1997, through December 31, 2013, studied all Swedish citizens born between 1982 and 1998 who were 15 years and older (N = 1 850 252). Individuals who emigrated from Sweden before the age of 15 years (n = 104 051) or immigrated to Sweden after the age of 13 years (ie, <2 years before the beginning of the follow-up; n = 22 009) were excluded. Data analysis was performed from April 21, 2016, to June 4, 2016. EXPOSURES Receipt of self-harm-associated clinical care. MAIN OUTCOMES AND MEASURES Conviction of a violent crime according to the Swedish penal code. RESULTS The study cohort consisted of 1 850 525 individuals (950 382 males and 900 143 females), and the mean (SD) follow-up time was 8.1 (4.7) years (range, 0-17.0 years; minimum age, 15 years; maximum age, 32 years). During a mean follow-up period of 8.1 years, 55 185 individuals (3.0%) received clinical care for self-harm. The crude hazard ratio was 4.9 (95% CI, 4.8-5.0) for violent crime conviction in exposed individuals compared with the unexposed group. Women who self-harm were at particularly high risk for expressing violent behaviors. After adjustment for relevant psychiatric comorbidities and socioeconomic status, an almost doubled hazard of violent offense remained (hazard ratio, 1.8; 95% CI, 1.8-1.9). CONCLUSIONS AND RELEVANCE Self-harm is associated with an increased risk of conviction for a violent offense in both sexes. The risk of violence, as well as the risk of suicide and self-harm, should be assessed among offending and self-harming individuals.

  • 4. Smeland, Olav B.
    et al.
    Frei, Oleksandr
    Kauppi, Karolina
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper. Department of Radiology, University of California San Diego, La Jolla; Center for Multimodal Imaging and Genetics, University of California San Diego, La Jolla.
    Hill, W. David
    Li, Wen
    Wang, Yunpeng
    Krull, Florian
    Bettella, Francesco
    Eriksen, Jon A.
    Witoelar, Aree
    Davies, Gail
    Fan, Chun C.
    Thompson, Wesley K.
    Lam, Max
    Lencz, Todd
    Chen, Chi-Hua
    Ueland, Torill
    Jönsson, Erik G.
    Djurovic, Srdjan
    Deary, Ian J.
    Dale, Anders M.
    Andreassen, Ole A.
    Identification of Genetic Loci Jointly Influencing Schizophrenia Risk and the Cognitive Traits of Verbal-Numerical Reasoning, Reaction Time, and General Cognitive Function2017Inngår i: JAMA psychiatry, ISSN 2168-6238, E-ISSN 2168-622X, Vol. 74, nr 10, s. 1065-1075Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    IMPORTANCE Schizophrenia is associated with widespread cognitive impairments. Although cognitive deficits are one of the factors most strongly associated with functional outcome in schizophrenia, current treatment strategies largely fail to ameliorate these impairments. To develop more efficient treatment strategies in patients with schizophrenia, a better understanding of the pathogenesis of these cognitive deficits is needed. Accumulating evidence indicates that genetic risk of schizophrenia may contribute to cognitive dysfunction. OBJECTIVE To identify genomic regions jointly influencing schizophrenia and the cognitive domains of reaction time and verbal-numerical reasoning, aswell as general cognitive function, a phenotype that captures the shared variation in performance across cognitive domains. DESIGN, SETTING, AND PARTICIPANTS Combining data from genome-wide association studies from multiple phenotypes using conditional false discovery rate analysis provides increased power to discover genetic variants and could elucidate shared molecular genetic mechanisms. Data from the following genome-wide association studies, published from July 24, 2014, to January 17, 2017, were combined: schizophrenia in the Psychiatric Genomics Consortium cohort (n = 79 757 [ cases, 34 486; controls, 45 271]); verbal-numerical reasoning (n = 36 035) and reaction time (n = 111 483) in the UK Biobank cohort; and general cognitive function in CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) (n = 53 949) and COGENT (Cognitive Genomics Consortium) (n = 27 888). MAIN OUTCOMES AND MEASURES Genetic loci identified by conditional false discovery rate analysis. Brain messenger RNA expression and brain expression quantitative trait locus functionality were determined. RESULTS Among the participants in the genome-wide association studies, 21 loci jointly influencing schizophrenia and cognitive traits were identified: 2 loci shared between schizophrenia and verbal-numerical reasoning, 6 loci shared between schizophrenia and reaction time, and 14 loci shared between schizophrenia and general cognitive function. One locus was shared between schizophrenia and 2 cognitive traits and represented the strongest shared signal detected (nearest gene TCF20; chromosome 22q13.2), and was shared between schizophrenia (z score, 5.01; P = 5.53 x 10(-7)), general cognitive function (z score, - 4.43; P = 9.42 x 10(-6)), and verbal-numerical reasoning (z score, - 5.43; P = 5.64 x 10(-8)). For 18 loci, schizophrenia risk alleles were associated with poorer cognitive performance. The implicated genes are expressed in the developmental and adult human brain. Replicable expression quantitative trait locus functionality was identified for 4 loci in the adult human brain. CONCLUSIONS AND RELEVANCE The discovered loci improve the understanding of the common genetic basis underlying schizophrenia and cognitive function, suggesting novel molecular genetic mechanisms.

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