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  • 1.
    Blom, Victoria
    et al.
    Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Bergström, Gunnar
    Division of Intervention and Implementation Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Hallsten, Lennart
    Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Bodin, Lennart
    Division of Intervention and Implementation Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Svedberg, Pia
    Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Genetic susceptibility to burnout in a Swedish twin cohort2012In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 27, no 3, p. 225-231Article in journal (Refereed)
    Abstract [en]

    Most previous studies of burnout have focused on work environmental stressors, while familial factors so far mainly have been overlooked. The aim of the study was to estimate the relative importance of genetic influences on burnout (measured with Pines Burnout Measure) in a sample of monozygotic (MZ) and dizygotic (DZ) Swedish twins. The study sample consisted of 20,286 individuals, born 1959–1986 from the Swedish twin registry who participated in the cross-sectional study of twin adults: genes and environment. Probandwise concordance rates (the risk for one twin to be affected given that his/her twin partner is affected by burnout) and within pair correlations were calculated for MZ and DZ same—and opposite sexed twin pairs. Heritability coefficients i.e. the proportion of the total variance attributable to genetic factors were calculated using standard biometrical model fitting procedures. The results showed that genetic factors explained 33% of the individual differences in burnout symptoms in women and men. Environmental factors explained a substantial part of the variation as well and are thus important to address in rehabilitation and prevention efforts to combat burnout.

  • 2.
    Brooke, Hannah Louise
    et al.
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Talback, Mats
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Hörnblad, Jesper
    National Board of Health and Welfare, Stockholm, Sweden.
    Johansson, Lars Age
    Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, United States.
    Druid, Henrik
    Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Feychting, Maria
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ljung, Rickard
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    The Swedish cause of death register2017In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 32, no 9, p. 765-773Article in journal (Refereed)
    Abstract [en]

    Sweden has a long tradition of recording cause of death data. The Swedish cause of death register is a high quality virtually complete register of all deaths in Sweden since 1952. Although originally created for official statistics, it is a highly important data source for medical research since it can be linked to many other national registers, which contain data on social and health factors in the Swedish population. For the appropriate use of this register, it is fundamental to understand its origins and composition. In this paper we describe the origins and composition of the Swedish cause of death register, set out the key strengths and weaknesses of the register, and present the main causes of death across age groups and over time in Sweden. This paper provides a guide and reference to individuals and organisations interested in data from the Swedish cause of death register.

  • 3.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Valdimarsdottir, Unnur
    Centre of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Epidemiology, Harvard TH Chan School of Public Health, Boston MA, USA.
    Stress and cancer: Nordic pieces to the complex puzzle2015In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 30, no 7, p. 525-527Article in journal (Other academic)
  • 4.
    Lagerros, Ylva Trolle
    et al.
    Unit of Clinical Epidemiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Cnattingius, Sven
    Unit of Clinical Epidemiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Granath, Fredrik
    Unit of Clinical Epidemiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Hanson, Ulf
    Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden.
    Wikström, Anna-Karin
    Unit of Clinical Epidemiology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden.
    From infancy to pregnancy: birth weight, body mass index, and the risk of gestational diabetes2012In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 27, no 10, p. 799-805Article in journal (Refereed)
    Abstract [en]

    Obesity is a risk factor for gestational diabetes, whereas the role of the mother's birth weight is more uncertain. We aimed to investigate the combined effect of mothers' birth-weight-for-gestational-age and early pregnancy Body Mass Index (BMI) in relation to risk of gestational diabetes. Between 1973 and 2006, we identified a cohort of 323,083 women included in the Swedish Medical Birth Register both as infants and as mothers. Main exposures were mothers' birth-weight-for-gestational-age (categorized into five groups according to deviation from national mean birth weight) and early pregnancy BMI (classified according to WHO). Rates of gestational diabetes increased with adult BMI, independently of birth-weight-for-gestational-age. However, compared to women with appropriate birth-weight-for-gestational-age [appropriate-for-gestational age (AGA); -1 to +1 SD] and BMI (<25.0), women with obesity class II-III (BMI ≥ 35.0) had an adjusted odds ratio (OR) of 28.7 (95 % confidence interval, CI 17.0-48.6) for gestational diabetes if they were born small-for-gestational-age [small for gestational age (SGA); <-2SD], OR = 20.3 (95 % CI 11.8-34.7) if born large-for-gestational-age [large-for-gestational-age (LGA); >2SD], and OR = 10.4 (95 % CI 8.4-13.0) if born AGA. Risk of gestational diabetes is not only increased among obese women, but also among women born SGA and LGA. Severely obese women born with a low or a high birth-weight-for-gestational-age seem more vulnerable to the development of gestational diabetes compared to normal weight women. Normal pre-pregnancy BMI diminishes the increased risk birth size may confer in terms of gestational diabetes. Therefore, the importance of keeping a healthy weight cannot be overemphasized.

  • 5.
    Ludvigsson, Jonas F.
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital.
    Lebwohl, Benjamin
    Department of Medicine, College of Physicians and Surgeons, Columbia University, New York NY, United States.
    Rubio-Tapia, Alberto
    Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic College of Medicine, Rochester MN, United States.
    Murray, Joseph A.
    Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic College of Medicine, Rochester MN, United States.
    Green, Peter H. R.
    Department of Medicine, College of Physicians and Surgeons, Columbia University, New York NY, United States.
    Ekbom, Anders
    Department of Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
    Granath, Fredrik
    Department of Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
    Does celiac disease influence survival in lymphoproliferative malignancy?2013In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 28, no 6, p. 475-483Article in journal (Refereed)
    Abstract [en]

    Celiac disease (CD) is associated with both lymphoproliferative malignancy (LPM) and increased death from LPM. Research suggests that co-existing autoimmune disease may influence survival in LPM. Through Cox regression we examined overall and cause-specific mortality in 316 individuals with CD+LPM versus 689 individuals with LPM only. CD was defined as having villous atrophy according to biopsy reports at any of Sweden's 28 pathology departments, and LPM as having a relevant disease code in the Swedish Cancer Register. During follow-up, there were 551 deaths (CD: n = 200; non-CD: n = 351). Individuals with CD+LPM were at an increased risk of death compared with LPM-only individuals [adjusted hazard ratio (aHR) = 1.23; 95 % confidence interval (CI) = 1.02-1.48]. However, this excess risk was only seen in the first year after LPM diagnosis (aHR = 1.76), with HRs decreasing to 1.09 in years 2-5 after LPM diagnosis and to 0.90 thereafter. Individuals with CD and non-Hodgkin lymphoma (NHL) were at a higher risk of any death as compared with NHL-only individuals (aHR = 1.23; 95 % CI = 0.97-1.56). This excess risk was due to a higher proportion of T cell lymphoma in CD patients. Stratifying for T- and B cell status, the HR for death in individuals with CD+NHL was 0.77 (95 % CI = 0.46-1.31). In conclusion, we found no evidence that co-existing CD influences survival in individuals with LPM. The increased mortality in the first year after LPM diagnosis is related to the predominance of T-NHL in CD individuals. Individuals with CD+LPM should be informed that their prognosis is similar to that of individuals with LPM only. However, this study had low statistical power to rule our excess mortality in patients with CD and certain LPM subtypes.

  • 6.
    Ludvigsson, Jonas F.
    et al.
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lundholm, Cecilia
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Örtqvist, Anne K.
    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.
    No association between macrolide treatment in infancy and later pyloric stenosis in Sweden2016In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 31, no 3, p. 331-332Article in journal (Refereed)
  • 7.
    Ludvigsson, Jonas F.
    et al.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Paediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Clinical Sciences Building 2, City Hospital, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York NY, USA.
    Svedberg, Pia
    Division of Insurance Medicine, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Olén, Ola
    Clinical Epidemiology Unit, Department of Medicine Stockholm, Karolinska Institutet, Stockholm, Sweden.
    Bruze, Gustaf
    Clinical Epidemiology Unit, Department of Medicine Stockholm, Karolinska Institutet, Stockholm, Sweden.
    Neovius, Martin
    Clinical Epidemiology Unit, Department of Medicine Stockholm, Karolinska Institutet, Stockholm, Sweden.
    The longitudinal integrated database for health insurance and labour market studies (LISA) and its use in medical research2019In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 34, no 4, p. 423-437Article in journal (Refereed)
    Abstract [en]

    Education, income, and occupation are factors known to affect health and disease. In this review we describe the Swedish Longitudinal Integrated Database for Health Insurance and Labour Market Studies (LISA, Longitudinell Integrationsdatabas for Sjukforsakrings- och Arbetsmarknadsstudier). LISA covers the adult Swedish population aged16years registered on December 31 each year since 1990 (since 2010 individuals aged15years). The database was launched in response to rising levels of sick leave in the country. Participation in Swedish government-administered registers such as LISA is compulsory, and hence selection bias is minimized. The LISA database allows researchers to identify individuals who do not work because of injury, disease, or rehabilitation. It contains data on sick leave and disability pension based on calendar year. LISA also includes information on unemployment benefits, disposable income, social welfare payments, civil status, and migration. During 2000-2017, an average of 97,000 individuals immigrated to Sweden each year. This corresponds to about 1% of the Swedish population (10 million people in 2017). Data on occupation have a completeness of 95%. Income data consist primarily of income from employment, capital, and allowances, including parental allowance. In Sweden, work force participation is around 80% (2017: overall: 79.1%; men 80.3% and women 77.9%). Education data are available in>98% of all individuals aged 25-64years, with an estimated accuracy for highest attained level of education of 85%. Some information on civil status, income, education, and employment before 1990 can be obtained through the Population and Housing Census data (FoB, Folk- och bostadsrakningen).

  • 8.
    Ludvigsson, Jonas F.
    et al.
    Örebro University Hospital. Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden; Dept Pediat, Örebro University Hospital, Örebro, Sweden.
    Zugna, Daniela
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden; Dept Med Sci, Canc Epidemiol Unit, Univ Turin, Turin, Italy; CPO Piemonte, Turin, Italy..
    Cnattingius, Sven
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    Richiardi, Lorenzo
    Dept Med Sci, Canc Epidemiol Unit, Univ Turin, Turin, Italy; Cancer Prevention (CPO), Piemonte, Turin, Italy.
    Ekbom, Anders
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden.
    Ortqvist, Ake
    Dept Med, Infect Dis Unit, Karolinska Inst, Stockholm, Sweden; Dept Communicable Dis Control & Prevent, Stockholm Cty Council, Stockholm, Sweden.
    Persson, Ingemar
    Medical Products Agency, Uppsala, Sweden.
    Stephansson, Olof
    Dept Med, Clin Epidemiol Unit, Karolinska Inst, Stockholm, Sweden; Dept Womens & Childrens Hlth, Karolinska Hosp & Inst, Stockholm, Sweden.
    Influenza H1N1 vaccination and adverse pregnancy outcome2013In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 28, no 7, p. 579-588Article in journal (Refereed)
    Abstract [en]

    Although vaccines against influenza can reduce maternal morbidity and mortality, large-scale data on adverse effects in the offspring are scarce. Historical cohort study in Stockholm County, Sweden. We linked H1N1 vaccination data (Pandemrix(A (R)), a mono-valent AS03 adjuvanted H1N1 vaccine) with pregnancy and birth data from 21,087 women with singleton offspring conceived between February 2009 and January 2010 (vaccinated during pregnancy: n = 13,297 vs. unvaccinated: n = 7,790). Data were analysed by conceptualizing the observational cohort as a series of nested cohorts defined at each week of gestation. Logistic regression estimated odds ratios (ORs) for low birth weight (LBW, < 2,500 g), preterm birth (< 37 completed weeks), small-for-gestational age (SGA, < 10th percentile of the gestational age-specific birth weight within the cohort), low 5-min Apgar score (< 7), and caesarean section. Data were adjusted for potential confounders, including maternal age, body mass index, smoking, parity, civil status and comorbidities. Compared with infants of non-vaccinated women, infants of vaccinated women had similar adjusted ORs (95 % CI) for LBW (0.91; 0.79-1.04), preterm birth (0.99; 0.89-1.10), SGA (0.97; 0.90-1.05), low Apgar score (1.05, 0.84-1.31), and a marginal risk reduction for caesarean section (0.94, 0.89-0.99). H1N1 vaccination during pregnancy, using an AS03-adjuvanted vaccine, does not appear to adversely influence offspring risks of LBW, preterm birth, SGA, or low Apgar score. Our results suggest that this vaccine is safe for the offspring when used in different stages of pregnancy.

  • 9.
    Middeldorp, Christel M.
    et al.
    Child Health Research Centre, University of Queensland, Brisbane QLD, Australia; Child and Youth Mental Health Service, Children’s Health Queensland Hospital and Health Service, Brisbane QLD, Australia; Department of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Univ Penn, Perelman Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.;Univ Groningen, Univ Med Ctr Groningen, Dept Psychiat, Groningen, Netherlands.;Orebro Univ, Sch Med Sci, Orebro, Sweden.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford OX3 7LE, England.;RIKEN, Ctr Integrat Med Sci, Lab Endocrinol Metab & Kidney Dis, Yokohama, Kanagawa 2300045, Japan.;Orebro Univ, Sch Med Sci, Orebro, Sweden.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Tiemeier, Hen-Ning
    Univ Leipzig, Pediat Res Ctr, Dept Womens & Child Hlth, Leipzig, Germany; Univ Leipzig, IFB Adipos Dis, Leipzig, Germany; Univ N Carolina, Dept Genet, Chapel Hill NC, USA; Leiden Univ, Dept Clin Epidemiol, Med Ctr, Leiden, Netherlands; Erasmus MC, Child & Adolescent Psychiat, Rotterdam, Netherlands; Harvard Univ, Social & Behav Sci, Harvard TH Chan Sch Publ Hlth, Boston MA, USA.
    The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia: design, results and future prospects2019In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 34, no 3, p. 279-300Article in journal (Refereed)
    Abstract [en]

    The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.

  • 10.
    Stokkeland, Knut
    et al.
    Department of Medicine, Visby Hospital, Visby, Sweden; Department of Medicine, Gastroenterology and Hepatology Unit, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
    Hultcrantz, Rolf
    Department of Medicine, Gastroenterology and Hepatology Unit, Karolinska Institutet, Stockholm, Sweden; Division of Hepatology, Karolinska Hospital, Stockholm, Sweden.
    Ekbom, Anders
    Department of Medicine, Solna, Clinical Epidemiology Unit, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden.
    Höijer, Jonas
    Unit of Biostatistics, Institute of Environmental Medicine (IMM), Karolinska Institutet, Stockholm, Sweden.
    Bottai, Matteo
    Unit of Biostatistics, Institute of Environmental Medicine (IMM), Karolinska Institutet, Stockholm, Sweden.
    Stephansson, Olof
    Department of Medicine Solna, Clinical Epidemiology Unit, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden; Department of Women’s and Children’s Health, Karolinska Institute, Stockholm, Sweden.
    Pregnancy outcome in more than 5000 births to women with viral hepatitis: a population-based cohort study in Sweden2017In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 32, no 7, p. 617-625Article in journal (Refereed)
    Abstract [en]

    Previous studies have shown inconsistent results with respect to hepatitis B (HBV), hepatitis C (HCV) and pregnancy outcome. The aim of this study was to investigate pregnancy outcome in women with HBV or HCV. In a nationwide cohort of births between 2001 and 2011 we investigated the risks of adverse pregnancy outcomes in 2990 births to women with HBV and 2056 births to women with HCV using data from Swedish healthcare registries. Births to women without HBV (n = 1090 979), and births without HCV (n = 1091 913) served as population controls. Crude and adjusted relative risks (aRR) were calculated using Poisson regression analysis. Women with HCV were more likely to smoke (46.7 vs. 8.0%) and to have alcohol dependence (18.9 vs. 1.3%) compared with population controls. Most women with HBV were born in non-Nordic countries (91.9%). Maternal HCV was associated with a decreased risk of preeclampsia (aRR: 0.39, 95% CI: 0.24-0.64), but an increased risk of preterm birth (aRR: 1.32, 95% CI: 1.08-1.60) and late neonatal death (7-27 days: aRR: 3.79, 95% CI: 1.07-13.39) Preterm birth were also more common in mothers with HBV, aRR: 1.21 (95% CI: 1.02-1.45). Both HBV and HCV are risk factors for preterm birth, while HCV seems to be associated with a decreased risk for preeclampsia. Future studies should corroborate these findings.

  • 11.
    Ueda, Peter
    et al.
    Dept Med, Clin Epidemiol Unit, Karolinska Univ Hosp Solna, Karolinska Inst, Stockholm, Sweden.
    Cnattingius, Sven
    Dept Med, Clin Epidemiol Unit, Karolinska Univ Hosp Solna, Karolinska Inst, Stockholm, Sweden.
    Stephansson, Olof
    Dept Med, Clin Epidemiol Unit, Stockholm, Sweden; Dept Womens & Childrens Hlth, Karolinska Univ Hosp Solna, Karolinska Inst, Stockholm, Sweden.
    Ingelsson, Erik
    Dept Med Sci, Mol Epidemiol & Sci Life Lab, Uppsala Univ, Uppsala, Sweden.
    Ludvigsson, Jonas F.
    Örebro University Hospital. Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bonamy, Anna-Karin Edstedt
    Dept Med, Clin Epidemiol Unit, Karolinska Univ Hosp Solna, Karolinska Inst, Stockholm, Sweden; Dept Womens & Childrens Hlth, Karolinska Inst, Stockholm, Sweden.
    Cerebrovascular and ischemic heart disease in young adults born preterm: a population-based Swedish cohort study2014In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 29, no 4, p. 253-260Article in journal (Refereed)
    Abstract [en]

    Preterm birth is associated with overall cardiovascular mortality in young adulthood, but which specific conditions that underlie this association is unknown. We studied mortality and morbidity from cerebrovascular and ischemic heart disease in individuals born preterm. In a nationwide Swedish study, we included 1,306,943 individuals without congenital malformations born between 1983 and 1995, followed from 15 years of age to December 31st, 2010. Of these, 73,489 (5.6 %) were born preterm (< 37 weeks of gestation). Cox proportional hazards regression analysis was used to calculate hazard ratios (HR) with 95 % confidence intervals (CI), after adjusting for maternal characteristics and birth weight for gestational age. Of 955 incident cases of cerebrovascular disease, 58 (6.1 %) occurred in preterm born subjects. The corresponding numbers of ischemic heart disease cases were 180 and 13 (7.2 %), respectively. Birth before 32 weeks was associated with a nearly twofold increased risk of cerebrovascular disease; adjusted HR, (95 % CI) = 1.89 (1.01-3.54) compared to term born individuals, whereas individuals born at 32-36 weeks were not at increased risk. Preterm birth was not associated with later ischemic heart disease; no cases of ischemic heart disease were recorded among those born before 32 weeks and the HR (95 % CI) for those born at 32-36 weeks of gestation was 1.45 (0.81-2.57), compared to term-born individuals. Birth before 32 weeks is associated with increased risk of cerebrovascular disease in young adulthood. Our data suggest that cardiovascular health promotion in follow-up programs after very preterm birth may be beneficial.

  • 12.
    Verheul, Ingrid
    et al.
    Rotterdam School of Management, Erasmus University Rotterdam, Rotterdam, The Netherlands; Erasmus Research Institute of Management (ERIM), Erasmus University Rotterdam, Rotterdam, The Netherlands.
    Rietdijk, Wim
    Erasmus School of Economics, Erasmus University Rotterdam, Rotterdam, The Netherlands; Institute for Behavior and Biology (EURIBEB), Erasmus University Rotterdam, Rotterdam, The Netherlands.
    Block, Joern
    Universität Trier, Trier, Germany; Erasmus Research Institute of Management (ERIM), Erasmus University Rotterdam, Rotterdam, The Netherlands.
    Franken, Ingmar
    Institute of Psychology, Erasmus University Rotterdam, Rotterdam, The Netherlands.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Karolinska Institutet Center of Neurodevelopmental Disorders (KIND), Stockholm, Sweden.
    Thurik, Roy
    Erasmus School of Economics, Erasmus University Rotterdam, Rotterdam, The Netherlands; Institute for Behavior and Biology (EURIBEB), Erasmus University Rotterdam, Rotterdam, The Netherlands; Erasmus Research Institute of Management (ERIM), Erasmus University Rotterdam, Rotterdam, The Netherlands; Montpellier Business School, Montpellier, France.
    The association between attention-deficit/hyperactivity (ADHD) symptoms and self-employment2016In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 31, no 8, p. 793-801Article in journal (Refereed)
    Abstract [en]

    Attention-deficit/hyperactivity (ADHD) symptoms have been associated with the decision to become self-employed. Although these symptoms are generally regarded as disadvantageous, there may also be a bright side. To our knowledge, however, there has been no systematic, epidemiological evidence to support this claim. This paper examines the association between ADHD symptoms and self-employment in a population-based sample from the STAGE cohort of the Swedish Twin Registry (N = 7208). For replication, we used a sample of Dutch students who participated in the Global University Entrepreneurial Spirit Students' Survey (N = 13,112). In the Swedish sample, we found a positive association with self-employment for both general ADHD symptoms [odds ratio (OR) 1.13; 95 % confidence intervals (CI) 1.04-1.23] and hyperactivity symptoms [OR 1.19; 95 % CI 1.08-1.32], whereas no association was found for attention-deficit symptoms [OR 0.99; 95 % CI 0.89-1.10]. The positive association between hyperactivity and self-employment was replicated in the Dutch student sample [OR 1.09; 95 % CI 1.03-1.15]. Our results show that certain aspects of ADHD, in particular hyperactivity, can have a bright side, as they are positively associated with self-employment.

  • 13. Wiklund, Fredrik
    et al.
    Trolle Lageros, Ylva
    Chang, Ellen
    Bälter, Katarina
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Adami, Hans-Olov
    Grönberg, Henrik
    Lifetime total physical activity and prostate cancer risk: a population-based case-control study in Sweden2008In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 23, no 11, p. 739-746Article in journal (Refereed)
    Abstract [en]

    The etiologic role of physical activity in prostate cancer development is unclear. We assessed the association between lifetime total physical activity and prostate cancer risk in a Swedish population-based case–control study comprising 1,449 incident prostate cancer cases and 1,118 unaffected population controls. Information regarding physical activity was obtained via a self-administered questionnaire assessing occupational, household, and recreational activity separately at various ages throughout an individual’s lifetime. Clinical data (TNM-classification, Gleason sum and PSA) was obtained from linkage to the National Prostate Cancer Registry. Overall, we observed no association between lifetime total physical activity and prostate cancer risk (odds ratio [OR] = 1.04, 95% confidence interval [CI] = 0.77–1.41 for ≥49.7 vs. <41.9 metabolic equivalent-hours per day). There was a significantly increased risk of prostate cancer in the most active men compared with the least active men in household (OR = 1.44, 95% CI = 1.08–1.92) and recreational physical activity (OR = 1.56, 95% CI = 1.16–2.10). Comparing the most active with the least active men, total physical activity was not associated with either localized disease (OR = 0.95, 95% CI = 0.67–1.34) or advanced disease (OR = 1.19, 95% CI = 0.83–1.71). These findings do not support the hypothesis that physical activity uniformly protects against prostate cancer development.

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