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  • 1.
    Aarts, Clara
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Kylberg, Elisabeth
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Hornell, A
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Hofvander, Yngve
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Gebre-Medhin, Mehari
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Greiner, Ted
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    How exclusive is exclusive breastfeeding? A comparison of data since birth with current status data:  2000In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 29, no 6, p. 1041-1046Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    There is no accepted and widely used indicator for exclusive breastfeeding since birth. Indeed, the difference between 'current status' data on exclusive breastfeeding and data on 'exclusive breastfeeding since birth' is rarely recognized. We used data from a longitudinal study to examine this issue.

    METHODS:

    A descriptive longitudinal, prospective study design was used in which 506 mother-infant pairs were included. The mothers completed daily recordings on infant feeding during the first nine months after birth. A research assistant conducted fortnightly home visits with structured interviews. The resulting data on breastfeeding patterns are presented in two different ways: analysis of 'current status' data based on a single 24-hour recording of infant feeding at 2, 4 and 6 months of age, and analysis of data 'since birth', i.e. data on infant feeding for every day, starting from birth until the ages of 2, 4 and 6 months.

    RESULTS:

    A wide discrepancy between the results obtained from the two analyses was found. The difference in the exclusive breastfeeding rate was over 40 percentage points at both 2 and 4 months of age (92% versus 51% at 2 months and 73% versus 30% at 4 months) and 9 percentage points at 6 months (11% versus 1.8%).

    CONCLUSIONS:

    Current status indicators based on a 24-hour period may be inadequate and even misleading for many purposes. We propose that in many studies an indicator called 'exclusive breastfeeding since birth' could be added.

  • 2.
    Accordini, Simone
    et al.
    Univ Verona, Dept Diagnost & Publ Hlth, Unit Epidemiol & Med Stat, Verona, Italy.
    Calciano, Lucia
    Univ Verona, Dept Diagnost & Publ Hlth, Unit Epidemiol & Med Stat, Verona, Italy.
    Johannessen, Ane
    Univ Bergen, Dept Global Publ Hlth & Primary Care, Ctr Int Hlth, Bergen, Norway.
    Portas, Laura
    Univ Verona, Dept Diagnost & Publ Hlth, Unit Epidemiol & Med Stat, Verona, Italy.
    Benediktsdottir, Bryndis
    Univ Iceland, Fac Med, Reykjavik, Iceland.
    Bertelsen, Randi Jacobsen
    Univ Bergen, Dept Clin Sci, Bergen, Norway;Haukeland Hosp, Dept Occupat Med, Bergen, Norway.
    Braback, Lennart
    Umea Univ, Dept Publ Hlth & Clin Med, Div Occupat & Environm Med, Umea, Sweden.
    Carsin, Anne-Elie
    Ctr Res Environm Epidemiol CREAL, ISGlobal, Barcelona, Spain;UPF, Barcelona, Spain;CIBER Epidemiol & Salud PUbl CIBERESP, Barcelona, Spain.
    Dharmage, Shyamali C.
    Univ Verona, Dept Diagnost & Publ Hlth, Unit Epidemiol & Med Stat, Verona, Italy;Univ Melbourne, Sch Populat & Global Hlth, Melbourne, Vic, Australia.
    Dratva, Julia
    ZHAW Sch Hlth Profess, Inst Hlth Sci, Winterthur, Switzerland;Basel Univ, Swiss Trop & Publ Hlth Inst, Dept Epidemiol & Publ Hlth, Basel, Switzerland.
    Forsberg, Bertil
    Umea Univ, Dept Publ Hlth & Clin Med, Div Occupat & Environm Med, Umea, Sweden.
    Real, Francisco Gomez
    Univ Bergen, Dept Clin Sci, Bergen, Norway.
    Heinrich, Joachim
    Ludwig Maximilians Univ Munchen, Univ Hosp Munich, Inner City Clin, Inst & Outpatient Clin Occupat,Social & Environm, Munich, Germany.
    Holloway, John W.
    Univ Southampton, Fac Med, Human Dev & Hlth, Southampton, Hants, England.
    Holm, Mathias
    Univ Gothenburg, Sahlgrenska Acad, Dept Occupat & Environm Med, Gothenburg, Sweden.
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Lung- allergy- and sleep research.
    Jogi, Rain
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Lung- allergy- and sleep research. Tartu Univ Hosp, Lung Clin, Tartu, Estonia.
    Leynaert, Benedicte
    INSERM, Pathophysiol & Epidemiol Resp Dis, UMR 1152, Paris, France.
    Malinovschi, Andrei
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
    Marcon, Alessandro
    Univ Verona, Dept Diagnost & Publ Hlth, Unit Epidemiol & Med Stat, Verona, Italy.
    Martinez-Moratalla Rovira, Jesus
    CHUA, Hlth Serv Castilla La Mancha SESCAM, Pneumol Serv, Albacete, Spain;Univ Castilla La Mancha, Sch Med, Albacete, Spain.
    Raherison, Chantal
    Bordeaux Univ, INSERM, U1219, Bordeaux, France.
    Luis Sanchez-Ramos, Jose
    Univ Huelva, Dept Nursing, Huelva, Spain.
    Schlunssen, Vivi
    Aarhus Univ, Dept Publ Hlth, Aarhus, Denmark;Natl Res Ctr Working Environm, Copenhagen, Denmark.
    Bono, Roberto
    Univ Turin, Dept Publ Hlth & Pediat, Turin, Italy.
    Corsico, Angelo G.
    Univ Pavia, IRCCS San Matteo Hosp Fdn, Div Resp Dis, Pavia, Italy.
    Demoly, Pascal
    Univ Montpellier, Hop Arnaud Villeneuve, Dept Pneumol & Addictol, Montpellier, France;Sorbonne Univ, INSERM, IPLESP, Paris, France.
    Dorado Arenas, Sandra
    Galdakao Usansolo Hosp, Pulmonol Dept, Biscay, Spain.
    Nowak, Dennis
    Ludwig Maximilians Univ Munchen, Univ Hosp Munich, Inner City Clin, Inst & Outpatient Clin Occupat,Social & Environm, Munich, Germany;Comprehens Pneumol Ctr Munich, German Ctr Lung Res, Munich, Germany.
    Pin, Isabelle
    CHU Grenoble Alpes, Pediat, Grenoble, France;Inst Adv Biosci, INSERM 1209, Grenoble, France;Univ Grenoble Alpes, Grenoble, France.
    Weyler, Joost
    Univ Antwerp, Dept Epidemiol & Social Med, Antwerp, Belgium;Univ Antwerp, StatUA Stat Ctr, Antwerp, Belgium.
    Jarvis, Deborah
    Imperial Coll, Natl Heart & Lung Inst, Populat Hlth & Occupat Dis, London, England;Imperial Coll, MRC PHE Ctr Environm & Hlth, London, England.
    Svanes, Cecilie
    Univ Bergen, Dept Global Publ Hlth & Primary Care, Ctr Int Hlth, Bergen, Norway;Haukeland Hosp, Dept Occupat Med, Bergen, Norway.
    Ageing, Lungs European Cohorts A. L. E. C. Study
    A three-generation study on the association of tobacco smoking with asthma2018In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 47, no 4, p. 1106-1117Article in journal (Refereed)
    Abstract [en]

    Background: Mothers' smoking during pregnancy increases asthma risk in their offspring. There is some evidence that grandmothers' smoking may have a similar effect, and biological plausibility that fathers' smoking during adolescence may influence offspring's health through transmittable epigenetic changes in sperm precursor cells. We evaluated the three-generation associations of tobacco smoking with asthma. Methods: Between 2010 and 2013, at the European Community Respiratory Health Survey III clinical interview, 2233 mothers and 1964 fathers from 26 centres reported whether their offspring (aged <= 51 years) had ever had asthma and whether it had coexisted with nasal allergies or not. Mothers and fathers also provided information on their parents' (grandparents) and their own asthma, education and smoking history. Multilevel mediation models within a multicentre three-generation framework were fitted separately within the maternal (4666 offspring) and paternal (4192 offspring) lines. Results: Fathers' smoking before they were 15 [relative risk ratio (RRR) = 1.43, 95% confidence interval (CI): 1.01-2.01] and mothers' smoking during pregnancy (RRR = 1.27, 95% CI: 1.01-1.59) were associated with asthma without nasal allergies in their offspring. Grandmothers' smoking during pregnancy was associated with asthma in their daughters [odds ratio (OR) = 1.55, 95% CI: 1.17-2.06] and with asthma with nasal allergies in their grandchildren within the maternal line (RRR = 1.25, 95% CI: 1.02-1.55). Conclusions: Fathers' smoking during early adolescence and grandmothers' and mothers' smoking during pregnancy may independently increase asthma risk in offspring. Thus, risk factors for asthma should be sought in both parents and before conception.

  • 3. Accordini, Simone
    et al.
    Calciano, Lucia
    Johannessen, Ane
    Portas, Laura
    Benediktsdóttir, Bryndis
    Bertelsen, Randi Jacobsen
    Bråbäck, Lennart
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Carsin, Anne-Elie
    Dharmage, Shyamali C.
    Dratva, Julia
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Gomez Real, Francisco
    Heinrich, Joachim
    Holloway, John W.
    Holm, Mathias
    Janson, Christer
    Jögi, Rain
    Leynaert, Bénédicte
    Malinovschi, Andrei
    Marcon, Alessandro
    Martínez-Moratalla Rovira, Jesús
    Raherison, Chantal
    Sánchez-Ramos, José Luis
    Schlünssen, Vivi
    Bono, Roberto
    Corsico, Angelo G.
    Demoly, Pascal
    Dorado Arenas, Sandra
    Nowak, Dennis
    Pin, Isabelle
    Weyler, Joost
    Jarvis, Deborah
    Svanes, Cecilie
    A three-generation study on the association of tobacco smoking with asthma2018In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 47, no 4, p. 1106-1117Article in journal (Refereed)
    Abstract [en]

    Background: Mothers' smoking during pregnancy increases asthma risk in their offspring. There is some evidence that grandmothers' smoking may have a similar effect, and biological plausibility that fathers' smoking during adolescence may influence offspring's health through transmittable epigenetic changes in sperm precursor cells. We evaluated the three-generation associations of tobacco smoking with asthma.

    Methods: Between 2010 and 2013, at the European Community Respiratory Health Survey III clinical interview, 2233 mothers and 1964 fathers from 26 centres reported whether their offspring (aged ≤51 years) had ever had asthma and whether it had coexisted with nasal allergies or not. Mothers and fathers also provided information on their parents' (grandparents) and their own asthma, education and smoking history. Multilevel mediation models within a multicentre three-generation framework were fitted separately within the maternal (4666 offspring) and paternal (4192 offspring) lines.

    Results: Fathers' smoking before they were 15 [relative risk ratio (RRR) = 1.43, 95% confidence interval (CI): 1.01-2.01] and mothers' smoking during pregnancy (RRR = 1.27, 95% CI: 1.01-1.59) were associated with asthma without nasal allergies in their offspring. Grandmothers' smoking during pregnancy was associated with asthma in their daughters [odds ratio (OR) = 1.55, 95% CI: 1.17-2.06] and with asthma with nasal allergies in their grandchildren within the maternal line (RRR = 1.25, 95% CI: 1.02-1.55).

    Conclusions: Fathers' smoking during early adolescence and grandmothers' and mothers' smoking during pregnancy may independently increase asthma risk in offspring. Thus, risk factors for asthma should be sought in both parents and before conception.

  • 4.
    Agardh, E.E
    et al.
    Karolinska Institutet.
    Ahlbom, A
    Andersson, T
    Efendic, S
    Grill, V
    Hallqvist, Johan
    Department of Public Health Science, Division of Social Medicine, Karolinska Institutet, Stockholm, Sweden.
    Östenson, C.G
    Karolinska Institutet.
    Socio-economic position at three points in life in association with type 2 diabetes and impaired glucose tolerance in middle-aged Swedish men and women2007In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 36, no 1, p. 84-92Article in journal (Refereed)
    Abstract [en]

    Background

    It has been suggested that low socio-economic position(SEP) during childhood and adolescence predicts risk of adulttype 2 diabetes. We investigated the associations between type2 diabetes and childhood SEP (fathers’ occupational position),participants’ education and adult SEP (participants’occupational position). To determine possible independent associationsbetween early SEP (fathers’ occupational position andparticipants’ education) and disease, we adjusted foradult SEP and factors present in adult life associated withtype 2 diabetes.

     

    Methods

    This cross-sectional study comprised 3128 men and 4821women aged 35–56 years. All subjects have gone througha health examination and answered a questionnaire on lifestylefactors. At the health centre, an oral glucose tolerance testwas administered and identified 55 men and 52 women with previouslyundiagnosed type 2 diabetes. Relative risks (RRs) with 95% CIswere calculated in multiple logistic regression analyses.

     

    Results

    The age-adjusted RRs of type 2 diabetes if having afather with middle occupational position were 2.3 [Confidenceinterval (CI:1.0–5.1) for women and, 2.0 (CI:0.7–5.6)for men]. Moreover, low education was associated with type 2diabetes in women, RR = 2.5 (CI:1.2–4.9). Low occupationalposition in adulthood was associated with type 2 diabetes inwomen, RR = 2.7 (CI:1.3–5.9) and men, RR = 2.9 (CI:1.5–5.7).The associations between early SEP and type 2 diabetes disappearedafter adjustment for adult SEP and factors associated with type2 diabetes.

     

    Conclusion

    The association between type 2 diabetes and low SEPduring childhood and adolescence in middle-aged Swedish subjectsdisappeared after adjustment for adult SEP and adult risk factorsof diabetes.

  • 5. Agardh, Emilie
    et al.
    Allebeck, Peter
    Hallqvist, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine.
    Moradi, Tahereh
    Sidorchuk, Anna
    Type 2 diabetes incidence and socio-economic position: a systematic review and meta-analysis2011In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 40, no 3, p. 804-818Article, review/survey (Refereed)
    Abstract [en]

    Background We conducted a systematic review and meta-analysis, the first to our knowledge, summarizing and quantifying the published evidence on associations between type 2 diabetes incidence and socio-economic position (SEP) (measured by educational level, occupation and income) worldwide and when sub-divided into high-, middle- and low-income countries. Methods Relevant case-control and cohort studies published between 1966 and January 2010 were searched in PubMed and EMBASE using the keywords: diabetes vs educational level, occupation or income. All identified citations were screened by one author, and two authors independently evaluated and extracted data from relevant publications. Risk estimates from individual studies were pooled using random-effects models quantifying the associations. Results Out of 5120 citations, 23 studies, including 41 measures of association, were found to be relevant. Compared with high educational level, occupation and income, low levels of these determinants were associated with an overall increased risk of type 2 diabetes; [relative risk (RR) = 1.41, 95% confidence interval (CI): 1.28-1.51], (RR = 1.31, 95% CI: 1.09-1.57) and (RR = 1.40, 95% CI: 1.04-1.88), respectively. The increased risks were independent of the income levels of countries, although based on limited data in middle- and low-income countries. Conclusions The risk of getting type 2 diabetes was associated with low SEP in high-, middle- and low-income countries and overall. The strength of the associations was consistent in high-income countries, whereas there is a strong need for further investigation in middle- and low-income countries.

  • 6.
    Ahrens, W.
    et al.
    Leibniz Institute for Prevention Research and Epidemiology - BIPS, Bremen, Germany / Institute of Statistics, Bremen University, Bremen, Germany.
    Siani, A.
    Institute of Food Sciences, National Research Council, Avellino, Italy.
    Adan, R.
    Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands.
    De Henauw, S.
    Department of Public Health, Ghent University, Ghent, Belgium.
    Eiben, Gabriele
    Section for Epidemiology and Social Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Gwozdz, W.
    Department of Intercultural Communication and Management, Copenhagen Business School, Copenhagen, Denmark.
    Hebestreit, A.
    Leibniz Institute for Prevention Research and Epidemiology - BIPS, Bremen, Germany.
    Hunsberger, M.
    Section for Epidemiology and Social Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Kaprio, J.
    Department of Public Health, University of Helsinki, Institute for Molecular Medicine (FIMM), Helsinki, Finland.
    Krogh, V.
    Epidemiology and Prevention Unit, Fondazione IRCSS Istituto Nazionale dei Tumori, Milan, Italy.
    Lissner, L.
    Section for Epidemiology and Social Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Molnár, D.
    Department of Paediatrics, University of Pe´cs, Pe´cs, Hungary.
    Moreno, L. A.
    GENUD (Growth, Exercise, Nutrition and Development) Research Group, University of Zaragoza, Zaragoza, Spain.
    Page, A.
    Centre for Exercise, Nutrition & Health Sciences, University of Bristol, Bristol, UK.
    Picó, C.
    Laboratory of Molecular Biology, Nutrition and Biotechnology (Nutrigenomics), University of the Balearic Islands (UIB) and CIBER Fisiopatologıa de la Obesidad y Nutricion, Palma de Mallorca, Spain.
    Reisch, L.
    Department of Intercultural Communication and Management, Copenhagen Business School, Copenhagen, Denmark.
    Smith, R. M.
    Minerva Communications UK, Andover, UK.
    Tornaritis, M.
    Research and Education Institute of Child Health, Strovolos, Cyprus.
    Veidebaum, T.
    National Institute for Health Development, Tallinn, Estonia.
    Williams, G.
    Department of Politics, Philosophy and Religion, Lancaster University, Lancaster, UK.
    Pohlabeln, H.
    Leibniz Institute for Prevention Research and Epidemiology - BIPS, Bremen, Germany.
    Pigeot, I.
    Leibniz Institute for Prevention Research and Epidemiology - BIPS, Bremen, Germany / Institute of Statistics, Bremen University, Bremen, Germany.
    Cohort Profile: The transition from childhood to adolescence in European children-how I.Family extends the IDEFICS cohort2017In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 46, no 5, p. 1394-1395Article in journal (Refereed)
  • 7.
    Airaksinen, Jaakko
    et al.
    Univ Helsinki, Dept Psychol & Logoped, Med, Haartmaninkatu 3,PL 21, FIN-00014 Helsinki, Finland; Finnish Inst Occupat Hlth, Dept Occupat Hlth, Helsinki, Finland.
    Ervasti, Jenni
    Department of Occupational Health, Finnish Institute of Occupational Health, Helsinki, Finland.
    Pentti, Jaana
    Clinicum, University of Helsinki, Helsinki, Finland; Department of Public Health, University of Turku and Turku University Hospital, Turku, Finland.
    Oksanen, Tuula
    Department of Occupational Health, Finnish Institute of Occupational Health, Helsinki, Finland.
    Suominen, Sakari
    Department of Public Health, University of Turku and Turku University Hospital, Turku, Finland.
    Vahtera, Jussi
    Department of Public Health, University of Turku and Turku University Hospital, Turku, Finland.
    Virtanen, Marianna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Public Health. Department of Occupational Health, Finnish Institute of Occupational Health, Helsinki, Finland.
    Kivimäki, Mika
    Department of Occupational Health, Finnish Institute of Occupational Health, Helsinki, Finland; Clinicum, University of Helsinki, Helsinki, Finland; Department of Epidemiology and Public Health, University College London, London, UK.
    The effect of smoking cessation on work disability risk: a longitudinal study analysing observational data as non-randomized nested pseudo-trials2019In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 48, no 2, p. 415-422Article in journal (Refereed)
    Abstract [en]

    Background

    Smoking increases disability risk, but the extent to which smoking cessation reduces the risk of work disability is unclear. We used non-randomized nested pseudo-trials to estimate the benefits of smoking cessation for preventing work disability.

    Methods

    We analysed longitudinal data on smoking status and work disability [long-term sickness absence (≥90 days) or disability pension] from two independent prospective cohort studies—the Finnish Public Sector study (FPS) (n = 7393) and the Health and Social Support study (HeSSup) (n = 2701)—as ‘nested pseudo-trials’. All the 10 094 participants were smokers at Time 1 and free of long-term work disability at Time 2. We compared the work disability risk after Time 2 of the participants who smoked at Time 1 and Time 2 with that of those who quit smoking between these times.

    Results

    Of the participants in pseudo-trials, 2964 quit smoking between Times 1 and 2. During the mean follow-up of 4.8 to 8.6 years after Time 2, there were 2197 incident cases of work disability across the trials. Quitting smoking was associated with a reduced risk of any work disability [summary hazard ratio = 0.89, 95% confidence interval (CI) 0.81–0.98]. The hazard ratio for the association between quitting smoking and permanent disability pension (928 cases) was of similar magnitude, but less precisely estimated (0.91, 95% CI 0.81–1.02). Among the participants with high scores on the work disability risk score (top third), smoking cessation reduced the risk of disability pension by three percentage points. Among those with a low risk score (bottom third), smoking cessation reduced the risk by half a percentage point.

    Conclusions

    Our results suggest an approximately 10% hazard reduction of work disability as a result of quitting smoking.

  • 8. Alberts, Marianne
    et al.
    Dikotope, Sekgothe A
    Choma, Solomon R
    Masemola, Matshane L
    Modjadji, Sewela EP
    Mashinya, Felistas
    Burger, Sandra
    Cook, Ian
    Brits, Sanette J
    Byass, Peter
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health. MRC/Wits Rural Public Health and Health Transitions Research Unit (Agincourt), School of Public Health, University of the Witwatersrand, Johannesberg, South Africa.
    Health & Demographic Surveillance System Profile: The Dikgale Health and Demographic Surveillance System.2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, no 5, p. 1565-1571Article in journal (Refereed)
  • 9. Aleksandrova, Krasimira
    et al.
    Jenab, Mazda
    Leitzmann, Michael
    Bueno-de-Mesquita, Bas
    Kaaks, Rudolf
    Trichopoulou, Antonia
    Bamia, Christina
    Lagiou, Pagona
    Rinaldi, Sabina
    Freisling, Heinz
    Carayol, Marion
    Pischon, Tobias
    Drogan, Dagmar
    Weiderpass, Elisabete
    Jakszyn, Paula
    Overvad, Kim
    Dahm, Christina C.
    Tjonneland, Anne
    Bouton-Ruault, Marie-Christine
    Kuehn, Tilman
    Peppa, Eleni
    Valanou, Elissavet
    La Vecchia, Carlo
    Palli, Domenico
    Panico, Salvatore
    Sacerdote, Carlotta
    Agnoli, Claudia
    Tumino, Rosario
    May, Anne
    van Vulpen, Jonna
    Borch, Kristin Benjaminsen
    Oyeyemi, Sunday Oluwafemi
    Ramon Quiros, J.
    Bonet, Catalina
    Sanchez, Maria-Jose
    Dorronsoro, Miren
    Navarro, Carmen
    Barricarte, Aurelio
    van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Wennberg, Patrik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Key, Timothy J.
    Khaw, Kay-Tee
    Wareham, Nicholas
    Assi, Nada
    Ward, Heather A.
    Aune, Dagfinn
    Riboli, Elio
    Boeing, Heiner
    Physical activity, mediating factors and risk of colon cancer: insights into adiposity and circulating biomarkers from the EPIC cohort2017In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 46, no 6, p. 1823-1835Article in journal (Refereed)
    Abstract [en]

    There is convincing evidence that high physical activity lowers the risk of colon cancer; however, the underlying biological mechanisms remain largely unknown. We aimed to determine the extent to which body fatness and biomarkers of various biologically plausible pathways account for the association between physical activity and colon cancer. We conducted a nested case-control study in a cohort of 519 978 men and women aged 25 to 70 years followed from 1992 to 2003. A total of 713 incident colon cancer cases were matched, using risk-set sampling, to 713 controls on age, sex, study centre, fasting status and hormonal therapy use. The amount of total physical activity during the past year was expressed in metabolic equivalent of task [MET]-h/week. Anthropometric measurements and blood samples were collected at study baseline. High physical activity was associated with a lower risk of colon cancer: relative risk a parts per thousand<yen>91 MET-h/week vs < 91 MET-h/week = 0.75 [95% confidence interval (CI): 0.57 to 0.96]. In mediation analyses, this association was accounted for by waist circumference: proportion explained effect (PEE) = 17%; CI: 4% to 52%; and the biomarkers soluble leptin receptor (sOB-R): PEE = 15%; 95% CI: 1% to 50% and 5-hydroxyvitamin D (25[OH]D): PEE = 30%; 95% CI: 12% to 88%. In combination, these factors explained 45% (95% CI: 20% to 125%) of the association. Beyond waist circumference, sOB-R and 25[OH]D additionally explained 10% (95% CI: 1%; 56%) and 23% (95% CI: 6%; 111%) of the association, respectively. Promoting physical activity, particularly outdoors, and maintaining metabolic health and adequate vitamin D levels could represent a promising strategy for colon cancer prevention.

  • 10.
    Anantharaman, Devasena
    et al.
    Int Agcy Res Canc, Genet Epidemiol Grp, Lyon, France..
    Muller, David C.
    Int Agcy Res Canc, Genet Epidemiol Grp, Lyon, France..
    Lagiou, Pagona
    Univ Athens, Sch Med, Dept Hyg Epidemiol & Med Stat, Athens, Greece..
    Ahrens, Wolfgang
    BIPS, Leibniz Inst Prevent Res & Epidemiol, Bremen, Germany.;Univ Bremen, Fac Math & Comp Sci, Bremen, Germany..
    Holcatova, Ivana
    Charles Univ Prague, Fac Med 1, Inst Hyg & Epidemiol, Prague, Czech Republic..
    Merletti, Franco
    Univ Turin, Dept Med Sci, Canc Epidemiol Unit, Turin, Italy..
    Kjaerheim, Kristina
    Canc Registry Norway, Oslo, Norway..
    Polesel, Jerry
    CRO Aviano Natl Canc Inst, Unit Epidemiol & Biostat, Aviano, Italy..
    Simonato, Lorenzo
    Univ Padua, Dept Mol Med, Lab Publ Hlth & Populat Studies, Padua, Italy..
    Canova, Cristina
    Univ Padua, Dept Mol Med, Lab Publ Hlth & Populat Studies, Padua, Italy..
    Castellsague, Xavier
    CIBERESP, IDIBELL, ICO, Unit Infect & Canc, Barcelona, Spain..
    Macfarlane, Tatiana V.
    Univ Aberdeen, Sch Med & Dent, Aberdeen, Scotland..
    Znaor, Ariana
    Croatian Natl Inst Publ Hlth, Croatian Natl Canc Registry, Zagreb, Croatia.;Int Agcy Res Canc, Sect Canc Surveillance, Lyon, France..
    Thomson, Peter
    Newcastle Univ, Ctr Oral Hlth Res, Newcastle Upon Tyne, Tyne & Wear, England..
    Robinson, Max
    Newcastle Univ, Ctr Oral Hlth Res, Newcastle Upon Tyne, Tyne & Wear, England..
    Conway, David I.
    Univ Glasgow, Sch Dent, Coll Med Vet & Life Sci, Glasgow, Lanark, Scotland..
    Healy, Claire M.
    Trinity Coll Dublin, Sch Dent Sci, Dublin, Ireland..
    Tjönneland, Anne
    Danish Canc Soc, Inst Canc Epidemiol, Copenhagen, Denmark..
    Westin, Ulla
    Lund Univ, Dept Otorhinolaryngol Malmo & Lund, Lund, Sweden..
    Ekström, Johanna
    Lund Univ, Dept Clin Sci, Lund, Sweden..
    Chang-Claude, Jenny
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany..
    Kaaks, Rudolf
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany..
    Overvad, Kim
    Inst Publ Hlth, Aarhus, Denmark..
    Drogan, Dagmar
    German Inst Human Nutr Potsdam Rehbruecke DIfE, Nuthetal, Germany..
    Hallmans, Göran
    Umea Univ, Dept Biobank Res, Umea, Sweden..
    Laurell, Göran
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Otolaryngology and Head and Neck Surgery.
    Bueno-de-Mesquita, H. B.
    Natl Inst Publ Hlth & Environm RIVM, Dept Determinants Chron Dis DCD, Bilthoven, Netherlands.;Univ Med Ctr, Dept Gastroenterol & Hepatol, Utrecht, Netherlands.;Imperial Coll London, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.;Univ Malaya, Fac Med, Dept Social & Prevent Med, Kuala Lumpur, Malaysia..
    Peeters, Petra H.
    Univ Med Ctr, Julius Ctr Hlth Sci & Primary Care, Dept Epidemiol, Utrecht, Netherlands.;Imperial Coll London, Sch Publ Hlth, MRC PHE, London, England..
    Agudo, Antonio
    ICO, Unit Nutr & Canc, Barcelona, Spain..
    Larranaga, Nerea
    BIODonostia Res Inst, Basque Hlth Dept, Publ Hlth Div Gipuzkoa, San Sebastian, Spain.;CIBER Epidemiol & Publ Hlth CIBERESP, Madrid, Spain..
    Travis, Ruth C.
    Univ Oxford, Nuffield Dept Populat Hlth, Canc Epidemiol Unit, Oxford, England..
    Palli, Domenico
    Canc Res & Prevent Inst ISPO, Mol & Nutr Epidemiol Unit, Florence, Italy..
    Barricarte, Aurelio
    CIBER Epidemiol & Publ Hlth CIBERESP, Madrid, Spain.;Navarre Publ Hlth Inst, Pamplona, Spain..
    Trichopoulou, Antonia
    Hellen Hlth Fdn, Athens, Greece.;Acad Athens, Bur Epidemiol Res, Athens, Greece..
    George, Saitakis
    Univ Athens, Sch Med, Dept Hyg Epidemiol & Med Stat, Athens, Greece.;Hellen Hlth Fdn, Athens, Greece..
    Trichopoulos, Dimitrios
    Hellen Hlth Fdn, Athens, Greece.;Acad Athens, Bur Epidemiol Res, Athens, Greece.;Harvard Sch Publ Hlth, Dept Epidemiol, Boston, MA USA..
    Ramon Quiros, J.
    Publ Hlth Directorate Asturias, Oviedo, Spain..
    Grioni, Sara
    Fdn IRCCS, Ist Nazl Tumori, Epidemiol & Prevent Unit, Milan, Italy..
    Sacerdote, Carlotta
    Univ Turin, Citta Salute & Sci Hosp, Canc Epidemiol Unit, Turin, Italy.;Ctr Canc Prevent CPO, Turin, Italy..
    Navarro, Carmen
    CIBER Epidemiol & Publ Hlth CIBERESP, Madrid, Spain.;IMIB Arrixaca, Murcia Reg Hlth Council, Dept Epidemiol, Murcia, Spain.;Univ Murcia, Dept Hlth & Social Sci, Murcia, Spain..
    Sanchez, Maria-Jose
    CIBER Epidemiol & Publ Hlth CIBERESP, Madrid, Spain.;Univ Granada, Inst Invest Biosanitaria, Granada, Spain..
    Tumino, Rosario
    Civ MP Arezzo Hosp, Canc Registry, Asp Ragusa, Ragusa, Italy.;Civ MP Arezzo Hosp, Histopathol Unit, Asp Ragusa, Ragusa, Italy..
    Severi, Gianluca
    Human Genet Fdn HuGeF, Turin, Italy.;Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.;Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Vic 3010, Australia..
    Boutron-Ruault, Marie-Christine
    INSERM, Ctr Res Epidemiol & Populat Hlth CESP, Villejuif, France.;Univ Paris 11, Villejuif, France.;Inst Gustave Roussy, Villejuif, France..
    Clavel-Chapelon, Francoise
    INSERM, Ctr Res Epidemiol & Populat Hlth CESP, Villejuif, France.;Univ Paris 11, Villejuif, France.;Inst Gustave Roussy, Villejuif, France..
    Panico, Salvatore
    Univ Naples Federico II, Dipartimento Med Clin & Chirurgia, Naples, Italy..
    Weiderpass, Elisabete
    Arctic Univ Norway, Univ Tromso, Fac Hlth Sci, Dept Community Med, Tromso, Norway.;Canc Registry Norway, Oslo, Norway.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Folkhalsan Res Ctr, Dept Genet Epidemiol, Helsinki, Finland..
    Lund, Eiliv
    Arctic Univ Norway, Univ Tromso, Fac Hlth Sci, Dept Community Med, Tromso, Norway..
    Gram, Inger T.
    Arctic Univ Norway, Univ Tromso, Fac Hlth Sci, Dept Community Med, Tromso, Norway..
    Riboli, Elio
    Imperial Coll London, Sch Publ Hlth, London, England..
    Pawlita, Michael
    German Canc Res Ctr, Heidelberg, Germany..
    Waterboer, Tim
    German Canc Res Ctr, Heidelberg, Germany..
    Kreimer, Aimee R.
    NCI, NIH, Bethesda, MD 20892 USA..
    Johansson, Mattias
    Int Agcy Res Canc, Genet Epidemiol Grp, Lyon, France..
    Brennan, Paul
    Int Agcy Res Canc, Genet Epidemiol Grp, Lyon, France..
    Combined effects of smoking and HPV16 in oropharyngeal cancer2016In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 45, no 3, p. 752-761Article in journal (Refereed)
    Abstract [en]

    Background: Although smoking and HPV infection are recognized as important risk factors for oropharyngeal cancer, how their joint exposure impacts on oropharyngeal cancer risk is unclear. Specifically, whether smoking confers any additional risk to HPV-positive oropharyngeal cancer is not understood.

    Methods: Using HPV serology as a marker of HPV-related cancer, we examined the interaction between smoking and HPV16 in 459 oropharyngeal (and 1445 oral cavity and laryngeal) cancer patients and 3024 control participants from two large European multicentre studies. Odds ratios and credible intervals [CrI], adjusted for potential confounders, were estimated using Bayesian logistic regression.

    Results: Both smoking [odds ratio (OR [CrI]: 6.82 [4.52, 10.29]) and HPV seropositivity (OR [CrI]: 235.69 [99.95, 555.74]) were independently associated with oropharyngeal cancer. The joint association of smoking and HPV seropositivity was consistent with that expected on the additive scale (synergy index [CrI]: 1.32 [0.51, 3.45]), suggesting they act as independent risk factors for oropharyngeal cancer.

    Conclusions: Smoking was consistently associated with increase in oropharyngeal cancer risk in models stratified by HPV16 seropositivity. In addition, we report that the prevalence of oropharyngeal cancer increases with smoking for both HPV16-positive and HPV16-negative persons. The impact of smoking on HPV16-positive oropharyngeal cancer highlights the continued need for smoking cessation programmes for primary prevention of head and neck cancer.

  • 11. Anantharaman, Devasena
    et al.
    Muller, David C
    Lagiou, Pagona
    Ahrens, Wolfgang
    Holcátová, Ivana
    Merletti, Franco
    Kjærheim, Kristina
    Polesel, Jerry
    Simonato, Lorenzo
    Canova, Cristina
    Castellsague, Xavier
    Macfarlane, Tatiana V
    Znaor, Ariana
    Thomson, Peter
    Robinson, Max
    Conway, David I
    Healy, Claire M
    Tjønneland, Anne
    Westin, Ulla
    Ekström, Johanna
    Chang-Claude, Jenny
    Kaaks, Rudolf
    Overvad, Kim
    Drogan, Dagmar
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research.
    Laurell, Göran
    Bueno-de-Mesquita, H B
    Peeters, Petra H
    Agudo, Antonio
    Larrañaga, Nerea
    Travis, Ruth C
    Palli, Domenico
    Barricarte, Aurelio
    Trichopoulou, Antonia
    George, Saitakis
    Trichopoulos, Dimitrios
    Quirós, J Ramón
    Grioni, Sara
    Sacerdote, Carlotta
    Navarro, Carmen
    Sánchez, María-José
    Tumino, Rosario
    Severi, Gianluca
    Boutron-Ruault, Marie-Christine
    Clavel-Chapelon, Francoise
    Panico, Salvatore
    Weiderpass, Elisabete
    Lund, Eiliv
    Gram, Inger T
    Riboli, Elio
    Pawlita, Michael
    Waterboer, Tim
    Kreimer, Aimée R
    Johansson, Mattias
    Umeå University, Faculty of Medicine, Department of Biobank Research.
    Brennan, Paul
    Combined effects of smoking and HPV16 in oropharyngeal cancer2016In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 45, no 3, p. 752-761Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Although smoking and HPV infection are recognized as important risk factors for oropharyngeal cancer, how their joint exposure impacts on oropharyngeal cancer risk is unclear. Specifically, whether smoking confers any additional risk to HPV-positive oropharyngeal cancer is not understood.

    METHODS: Using HPV serology as a marker of HPV-related cancer, we examined the interaction between smoking and HPV16 in 459 oropharyngeal (and 1445 oral cavity and laryngeal) cancer patients and 3024 control participants from two large European multi-centre studies. Odds ratios and credible intervals [CrI], adjusted for potential confounders, were estimated using Bayesian logistic regression.

    RESULTS: Both smoking [odds ratio (OR [CrI]: 6.82 [4.52, 10.29]) and HPV seropositivity (OR [CrI]: 235.69 [99.95, 555.74]) were independently associated with oropharyngeal cancer. The joint association of smoking and HPV seropositivity was consistent with that expected on the additive scale (synergy index [CrI]: 1.32 [0.51, 3.45]), suggesting they act as independent risk factors for oropharyngeal cancer.

    CONCLUSIONS: Smoking was consistently associated with increase in oropharyngeal cancer risk in models stratified by HPV16 seropositivity. In addition, we report that the prevalence of oropharyngeal cancer increases with smoking for both HPV16-positive and HPV16-negative persons. The impact of smoking on HPV16-positive oropharyngeal cancer highlights the continued need for smoking cessation programmes for primary prevention of head and neck cancer.

  • 12. Andersson, T
    et al.
    Högberg, U
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynaecology.
    Bergström, S
    Community-based prevention of perinatal deaths: lessons from nineteenth-century Sweden.2000In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 29, no 3, p. 542-8Article in journal (Refereed)
    Abstract [en]

    Poor reproductive history, particularly previously high perinatal mortality, is associated with high perinatal mortality. Midwifery-assisted at home deliveries successfully reduced perinatal mortality.

  • 13.
    Arifeen, Shams El
    et al.
    Int Ctr Diarrhoeal Dis Res Icddr B, Dhaka, Bangladesh.
    Ekström, Eva-Charlotte
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH), International Child Health and Nutrition.
    Frongillo, Edward A
    Univ South Carolina, Arnold Sch Publ Hlth, Dept Hlth Promot Educ & Behav, Columbia, SC USA.
    Hamadani, Jena
    Int Ctr Diarrhoeal Dis Res Icddr B, Dhaka, Bangladesh.
    Khan, Ashraful Islam
    Int Ctr Diarrhoeal Dis Res Icddr B, Dhaka, Bangladesh.
    Naved, Ruchira T
    Int Ctr Diarrhoeal Dis Res Icddr B, Dhaka, Bangladesh.
    Rahman, Anisur
    Int Ctr Diarrhoeal Dis Res Icddr B, Dhaka, Bangladesh.
    Raqib, Rubhana
    Int Ctr Diarrhoeal Dis Res Icddr B, Dhaka, Bangladesh.
    Rasmussen, Kathleen M
    Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA.
    Ekholm Selling, Katarina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH), International Child Health and Nutrition.
    Wagatsuma, Yukiko
    Univ Tsukuba, Dept Med, Tsukuba, Ibaraki, Japan.
    Persson, Lars-Åke
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH), International Child Health and Nutrition. London Sch Hyg & Trop Med, Dept Dis Control, London, England.
    Cohort Profile: The Maternal and Infant Nutrition Interventions in Matlab (MINIMat) Cohort in Bangladesh2018In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 47, no 6, p. 1737-1738eArticle in journal (Refereed)
  • 14. Aschard, Hugues
    et al.
    Tobin, Martin D
    Hancock, Dana B
    Skurnik, David
    Sood, Akshay
    James, Alan
    Vernon Smith, Albert
    Manichaikul, Ani W
    Campbell, Archie
    Prins, Bram P
    Hayward, Caroline
    Loth, Daan W
    Porteous, David J
    Strachan, David P
    Zeggini, Eleftheria
    O'Connor, George T
    Brusselle, Guy G
    Boezen, H Marike
    Schulz, Holger
    Deary, Ian J
    Hall, Ian P
    Rudan, Igor
    Kaprio, Jaakko
    Wilson, James F
    Wilk, Jemma B
    Huffman, Jennifer E
    Hua Zhao, Jing
    de Jong, Kim
    Lyytikäinen, Leo-Pekka
    Wain, Louise V
    Jarvelin, Marjo-Riitta
    Kähönen, Mika
    Fornage, Myriam
    Polasek, Ozren
    Cassano, Patricia A
    Barr, R Graham
    Rawal, Rajesh
    Harris, Sarah E
    Gharib, Sina A
    Enroth, Stefan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Heckbert, Susan R
    Lehtimäki, Terho
    Gyllensten, Ulf B.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Society Scientific Group, Understanding
    Jackson, Victoria E
    Gudnason, Vilmundur
    Tang, Wenbo
    Dupuis, Josée
    Soler Artigas, María
    Joshi, Amit D
    London, Stephanie J
    Kraft, Peter
    Evidence for large-scale gene-by-smoking interaction effects on pulmonary function2017In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 46, no 3, p. 894-904Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Smoking is the strongest environmental risk factor for reduced pulmonary function. The genetic component of various pulmonary traits has also been demonstrated, and at least 26 loci have been reproducibly associated with either FEV1 (forced expiratory volume in 1 second) or FEV1/FVC (FEV1/forced vital capacity). Although the main effects of smoking and genetic loci are well established, the question of potential gene-by-smoking interaction effect remains unanswered. The aim of the present study was to assess, using a genetic risk score approach, whether the effect of these 26 loci on pulmonary function is influenced by smoking.

    METHODS: We evaluated the interaction between smoking exposure, considered as either ever vs never or pack-years, and a 26-single nucleotide polymorphisms (SNPs) genetic risk score in relation to FEV1 or FEV1/FVC in 50 047 participants of European ancestry from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) and SpiroMeta consortia.

    RESULTS: We identified an interaction (βint = -0.036, 95% confidence interval, -0.040 to -0.032, P = 0.00057) between an unweighted 26 SNP genetic risk score and smoking status (ever/never) on the FEV1/FVC ratio. In interpreting this interaction, we showed that the genetic risk of falling below the FEV 1: /FVC threshold used to diagnose chronic obstructive pulmonary disease is higher among ever smokers than among never smokers. A replication analysis in two independent datasets, although not statistically significant, showed a similar trend in the interaction effect.

    CONCLUSIONS: This study highlights the benefit of using genetic risk scores for identifying interactions missed when studying individual SNPs and shows, for the first time, that persons with the highest genetic risk for low FEV1/FVC may be more susceptible to the deleterious effects of smoking.

  • 15.
    Ashfaq, Awais
    et al.
    Halmstad University, School of Information Technology, Halmstad Embedded and Intelligent Systems Research (EIS), CAISR - Center for Applied Intelligent Systems Research.
    Lönn, Stefan
    Research and Development, Region Halland, Sweden.
    Nilsson, Håkan
    Economic Department, Region Halland, Sweden.
    Eriksson, Jonny
    Halland Hospital, Region Halland, Sweden.
    Kwatra, Japneet
    Brigham and Women’s Hospital, US.
    Yasin, Zayed
    Brigham and Women’s Hospital, US.
    Slutzman, Jonathan
    Massachusetts General Hospital, US.
    Wallenfeldt, Thomas
    CGI Group Inc. Consultants to Government and Industries, Sweden.
    Obermeyer, Ziad
    School of Public Health, University of California at Berkeley, US.
    Anderson, Philip
    Department of Emergency Medicine, Brigham & Women’s Hospital, Harvard Medical School, Boston, US..
    Lingman, Markus
    Halland Hospital, Region Halland, Sweden.
    Data Profile: Regional Healthcare Information Platform in Halland, Sweden2019In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685Article in journal (Refereed)
    Abstract [en]

    Accurate and comprehensive healthcare data coupled with modern analytical tools can play a vital role in enabling care providers to make better-informed decisions, leading to effective and cost-efficient care delivery. This paper describes a novel strategic healthcare analysis and research platform that encapsulates 360-degree pseudo-anonymized data covering clinical, operational capacity and financial data on over 500,000 patients treated since 2009 across all care delivery units in the county of Halland, Sweden. The over-arching goal is to develop a comprehensive healthcare data infrastructure that captures complete care processes at individual, organizational and population levels. These longitudinal linked healthcare data are a valuable tool for research in a broad range of areas including health economy and process development using real world evidence.

    Key messages

    Structured and standardized variables have been linked from different regional healthcare sources into a research information platform including all healthcare visits in the county of Halland in Sweden, from 2009 to date.

    Since 2015, the regional information platform integrates a cost component to each healthcare visit: thus being able to quantify patient level value, safety and cost efficiency across the continuum of care.

  • 16.
    B Almquist, Ylva
    et al.
    Stockholm University, Faculty of Social Sciences, Department of Public Health Sciences, Centre for Health Equity Studies (CHESS).
    Grotta, Alessandra
    Stockholm University, Faculty of Social Sciences, Department of Public Health Sciences, Centre for Health Equity Studies (CHESS).
    Vågerö, Denny
    Stockholm University, Faculty of Social Sciences, Department of Public Health Sciences, Centre for Health Equity Studies (CHESS).
    Stenberg, Sten-Åke
    Stockholm University, Faculty of Social Sciences, The Swedish Institute for Social Research (SOFI).
    Modin, Bitte
    Stockholm University, Faculty of Social Sciences, Department of Public Health Sciences, Centre for Health Equity Studies (CHESS).
    Cohort Profile Update: The Stockholm Birth Cohort Study2019In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685Article in journal (Refereed)
  • 17.
    Beckley, Amber L.
    et al.
    Stockholm University, Faculty of Social Sciences, Department of Criminology.
    Kuja-Halkola, Ralf
    Lundholm, Lena
    Långström, Niklas
    Frisell, Thomas
    Association of height and violent criminality: results from a Swedish total population study2014In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 43, no 3, p. 835-842Article in journal (Refereed)
    Abstract [en]

    Background: Violent criminality is at least moderately heritable, but the mechanisms behind this remain largely unexplained. Height, a highly heritable trait, may be involved but no study has estimated the effect of height on crime while simultaneously accounting for important demographic, biological and other heritable confounders. Methods: We linked nationwide, longitudinal registers for 760 000 men who underwent mandatory military conscription from 1980 through 1992 in Sweden, to assess the association between height and being convicted of a violent crime. We used Cox proportional hazard modelling and controlled for three types of potential confounders: physical characteristics, childhood demographics and general cognitive ability (intelligence). Results: In unadjusted analyses, height had a moderate negative relationship to violent crime; the shortest of men were twice as likely to be convicted of a violent crime as the tallest. However, when simultaneously controlling for all measured confounders, height was weakly and positively related to violent crime. Intelligence had the individually strongest mitigating effect on the height-crime relationship. Conclusions: Although shorter stature was associated with increased risk of violent offending, our analyses strongly suggested that this relationship was explained by intelligence and other confounding factors. Hence, it is unlikely that height, a highly heritable physical characteristic, accounts for much of the unexplained heritability of violent criminality.

  • 18. Bjorkenstam, Emma
    et al.
    Bjorkenstam, Charlotte
    Vinnerljung, Bo
    Hallqvist, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine.
    Ljung, Rickard
    Juvenile delinquency, social background and suicide-a Swedish national cohort study of 992 881 young adults2011In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 40, no 6, p. 1585-1592Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: As the suicide rates in young adults do not show a clear decline, it is important to elucidate possible risk factors. Juvenile delinquency has been pointed out as a possible risk behaviour.

    METHODS: This register-based cohort study comprises the birth cohorts between 1972 and 1981 in Sweden. We followed 992,881 individuals from the age of 20 years until 31 December 2006, generating 10 210 566 person-years and 1482 suicides. Juvenile delinquency was defined as being convicted of a crime between the ages of 15 and 19 years. Estimates of risk of suicide were calculated as incidence rate ratio (IRR) with 95% confidence intervals (CIs) using Poisson regression analysis with adjustment for potential confounding by their own and their parents' mental illness or substance abuse, parental education, single parenthood, social assistance, adoption and foster care.

    RESULTS: Among females, 5.9%, and among males, 17.9%, had at least one conviction between the ages 15 and 19 years. In the fully adjusted model, females with one conviction had a suicide risk of 1.7 times higher (95% CI 1.2-2.4), the corresponding IRR for men was 2.0 (95% CI 1.7-2.4) and 5.7 (95% CI 2.5-13.1) and 6.6 (95% CI 5.2-8.3), for women and men with five or more convictions. The effect of severe delinquency on suicide was independent of parental educational level.

    CONCLUSIONS: This study supports the hypothesis that individuals with delinquent behaviour in late adolescence have an increased risk of suicide as young adults. Regardless of causality issues, repeated juvenile offenders should be regarded by professionals in health, social and correctional services who come into contact with this group as a high-risk group for suicide.

  • 19. Björkenstam, Emma
    et al.
    Björkenstam, Charlotte
    Vinnerljung, Bo
    Stockholm University, Faculty of Social Sciences, Department of Social Work.
    Hallqvist, Johan
    Ljung, Rickard
    Juvenile delinquency, social background and suicide-a Swedish national cohort study of 992 881 young adults2011In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 40, no 6, p. 1585-1592Article in journal (Refereed)
    Abstract [en]

    Background As the suicide rates in young adults do not show a clear decline, it is important to elucidate possible risk factors. Juvenile delinquency has been pointed out as a possible risk behaviour. Methods This register-based cohort study comprises the birth cohorts between 1972 and 1981 in Sweden. We followed 992 881 individuals from the age of 20 years until 31 December 2006, generating 10 210 566 person-years and 1482 suicides. Juvenile delinquency was defined as being convicted of a crime between the ages of 15 and 19 years. Estimates of risk of suicide were calculated as incidence rate ratio (IRR) with 95% confidence intervals (CIs) using Poisson regression analysis with adjustment for potential confounding by their own and their parents' mental illness or substance abuse, parental education, single parenthood, social assistance, adoption and foster care. Results Among females, 5.9%, and among males, 17.9%, had at least one conviction between the ages 15 and 19 years. In the fully adjusted model, females with one conviction had a suicide risk of 1.7 times higher (95% CI 1.2-2.4), the corresponding IRR for men was 2.0 (95% CI 1.7-2.4) and 5.7 (95% CI 2.5-13.1) and 6.6 (95% CI 5.2-8.3), for women and men with five or more convictions. The effect of severe delinquency on suicide was independent of parental educational level. Conclusions This study supports the hypothesis that individuals with delinquent behaviour in late adolescence have an increased risk of suicide as young adults. Regardless of causality issues, repeated juvenile offenders should be regarded by professionals in health, social and correctional services who come into contact with this group as a high-risk group for suicide.

  • 20. Bjørge, Tone
    et al.
    Lukanova, Annekatrin
    Tretli, Steinar
    Manjer, Jonas
    Ulmer, Hanno
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Selmer, Randi
    Nagel, Gabriele
    Almquist, Martin
    Concin, Hans
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. null.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. null.
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. null.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. null.
    Engeland, Anders
    null.
    Metabolic risk factors and ovarian cancer in the metabolic syndrome and cancer project2011In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 40, no 6, p. 1667-1677Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: No studies have so far evaluated the impact of the metabolic syndrome (MetS) as an entity on ovarian cancer risk. The authors aimed to examine the association between factors in the MetS, individually and combined, and risk of ovarian cancer incidence and mortality. METHODS: Altogether, 290 000 women from Austria, Norway and Sweden were enrolled during 1974-2005, with measurements taken of height, weight, blood pressure and levels of glucose, cholesterol and triglycerides. Relative risks (RRs) of ovarian cancer were estimated using Cox regression for each MetS factor in quintiles and for standardized levels (z-scores), and for a composite z-score for the MetS. RRs were corrected for random error in measurements. RESULTS: During follow-up, 644 epithelial ovarian cancers and 388 deaths from ovarian cancer were identified. There was no overall association between MetS and ovarian cancer risk. Increasing levels of cholesterol [RR 1.52, 95% confidence interval (95% CI) 1.01-2.29, per 1-U increment of z-score] and blood pressure (RR 1.79, 95% CI 1.12-2.86) conferred, however, increased risks of mucinous and endometrioid tumours, respectively. In women below the age of 50 years, there was increased risk of ovarian cancer mortality for MetS (RR 1.52, 95% CI 1.00-2.30). Increasing levels of BMI (RR 1.17, 95% CI 1.01-1.37) conferred increased risk of ovarian cancer mortality in women above the age of 50 years. CONCLUSION: There was no overall association between MetS and ovarian cancer risk. However, increasing levels of cholesterol and blood pressure increased the risks of mucinous and endometrioid tumours, respectively. Increasing levels of BMI conferred an increased risk of ovarian cancer mortality in women above the age of 50 years.

  • 21.
    Bonn, S. E.
    et al.
    Karolinska Inst, Stockholm, Sweden..
    Wiklund, F.
    Karolinska Inst, Stockholm, Sweden..
    Sjolander, A.
    Karolinska Inst, Stockholm, Sweden..
    Szulkin, R.
    Karolinska Inst, Stockholm, Sweden..
    Stattin, P.
    Umea Univ, Umea, Sweden..
    Holmberg, E.
    Univ Gothenburg, Sahlgrenska Acad, Gothenburg, Sweden..
    Gronberg, H.
    Karolinska Inst, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Stockholm, Sweden..
    Body Mass Index and Weight Change in Men with Prostate Cancer: Progression and Mortality.2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, p. 141-142Article in journal (Other academic)
  • 22. Bonn, S. E.
    et al.
    Wiklund, F.
    Sjölander, A.
    Szulkin, R.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Holmberg, E.
    Grönberg, H.
    Bälter, K.
    Body Mass Index and Weight Change in Men with Prostate Cancer: Progression and Mortality2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, p. 141-142Article in journal (Other academic)
  • 23.
    Brew, Bronwyn K.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lundholm, Cecilia
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Viktorin, Alexander
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York NY, 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.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; School of Medical Sciences, Örebro University, Örebro, Sweden.
    Longitudinal depression or anxiety in mothers and offspring asthma: a Swedish population-based study2018In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 47, no 1, p. 166-174Article in journal (Refereed)
    Abstract [en]

    Background: Previous research has found that maternal stress during pregnancy increases the risk of offspring asthma. However, whether this association is consistent with a causal interpretation has never been tested. The objective is to determine whether there is a critical exposure period for maternal depression or anxiety on offspring asthma or whether cumulative exposure is most important, and to investigate evidence of confounding.

    Methods: The study population included all children born in Sweden from July 2006 to December 2009 (n = 360 526). Information about childhood asthma, maternal depression or anxiety (diagnosis or medication) and covariates was obtained from the Swedish national health registers. The associations between exposure periods (pre-conception, pregnancy, postnatal or current) and childhood asthma were estimated using structured life course approach hypothesis testing. Paternal and cousin analyses were used to test for evidence of confounding from shared genes and environment.

    Results: For childhood asthma, cumulative exposure best described the effect of exposure to maternal depression or anxiety up to a maximum of any two exposure periods [adjusted odds ratio 1.44, 95% confidence interval (CI) 1.38, 1.52]. The hypotheses of a critical period were not supported. The paternal and cousin analyses indicated minimal influence from familial confounding.

    Conclusions: These findings support an association between cumulative exposure to maternal depression or anxiety and asthma development in offspring. This association is unique for maternal depression or anxiety and not due to familial confounding. The clinical implication is that effective psychological management of women with chronic distress may reduce offspring asthma risk.

  • 24.
    Brännström, Inger
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Weinehall, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Persson, Lars Åke
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Wester, P O
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Wall, Stig
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Changing social patterns of risk factors for cardiovascular disease in a Swedish community intervention programme1993In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 22, no 6, p. 1026-1037Article in journal (Refereed)
    Abstract [en]

    Since 1985 a small-scale community-based cardiovascular disease (CVD) preventive programme has been in operation in an inland municipality, Norsjö, in Northern Sweden. The aim of this study was to assess the development of the relationship between social position and CVD risk factors in repeated cross-sectional surveys (1985-1990) among all men and women aged 30, 40, 50 and 60 years in the study area, using an age-stratified random sample from the Northern Sweden MONICA Study of 1986 and 1990 as reference population. These multiple cross-sectional surveys comprised a self-administered questionnaire and a health examination. Of the study population 95% (n = 1499) and 80% of those in the reference area (n = 3208) participated. Subjects were classified with regard to demographic, structural and social characteristics in relation to CVD risk factors and self-reported health status. Time trends in classical risk factor occurrence were assessed in terms of age- and sex- adjusted odds ratios using Mantel-Haenszel procedures. When simultaneously adjusting for several potential confounders we used a logistic regression analysis. Initially, more than half of the study population, both males and females, had and elevated (> or = 6.5 mmol/l) serum cholesterol level. After adjustments had been made for age and social factors it was found that the relative risk of hypercholesterolaemia dropped substantially and significantly among both sexes during the 6 years of CVD intervention in the study area. However, the probability of being a smoker was significantly reduced only in highly educated groups. Among other risk factors no single statistically significant change over time could be found. In the reference area there were no changes over time for the selected CVD risk factors. People in the study area had a less favourable perception of their health than those in the reference area. Social differences were found when perceived good health was measured, especially in variables indicating emotional and social support. When sex, age and social factors had been accounted for there was not clear change over the years in perceived good health.

  • 25. Cameron, Adrian J.
    et al.
    Magliano, Dianna J.
    Shaw, Jonathan E.
    Zimmet, Paul Z.
    Carstensen, Bendix
    Alberti, K. George M. M.
    Tuomilehto, Jaakko
    Barr, Elizabeth L. M.
    Pauvaday, Vassen K.
    Kowlessur, Sudhirsen
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    The influence of hip circumference on the relationship between abdominal obesity and mortality2012In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 41, no 2, p. 484-494Article in journal (Refereed)
    Abstract [en]

    Background Higher waist circumference and lower hip circumference are both associated with increased cardiovascular disease (CVD) risk, despite being directly correlated. The real effects of visceral obesity may therefore be underestimated when hip circumference is not fully taken into account. We hypothesized that adding waist and hip circumference to traditional risk factors would significantly improve CVD risk prediction. Methods In a population-based survey among South Asian and African Mauritians (n = 7978), 1241 deaths occurred during 15 years of follow-up. In a model that included variables used in previous CVD risk calculations (a Framingham-type model), the association between waist circumference and mortality was examined before and after adjustment for hip circumference. The percentage with an increase in estimated 10-year cumulative mortality of > 25% and a decrease of > 20% after waist and hip circumference were added to the model was calculated. Results Waist circumference was strongly related to mortality only after adjustment for hip circumference and vice versa. Adding waist and hip circumference to a Framingham-type model increased estimated 10-year cumulative CVD mortality by > 25% for 23.7% of those who died and 15.7% of those censored. Cumulative mortality decreased by > 20% for 4.5% of those who died and 14.8% of those censored. Conclusions The effect of central obesity on mortality risk is seriously underestimated without adjustment for hip circumference. Adding waist and hip circumference to a Framingham-type model for CVD mortality substantially increased predictive power. Both may be important inclusions in CVD risk prediction models.

  • 26.
    Carlson, Per
    Mid Sweden University.
    Commentary: Russia's mortality crisis, alcohol and social transformation2009In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 38, no 1, p. 156-157Article in journal (Refereed)
  • 27.
    Carlson, Per
    Mid Sweden University, Faculty of Human Sciences, Department of Social Sciences.
    Commentary: Russia's mortality crisis, alcohol and social transformation2009In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 38, no 1, p. 156-157Article in journal (Other academic)
  • 28.
    Chang, Zheng
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Psychiatry, University of Oxford, Oxford, UK.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M´.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    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.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Maternal age at childbirth and risk for ADHD in offspring: a population-based cohort study2014In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 43, no 6, p. 1815-1824Article in journal (Refereed)
    Abstract [en]

    Background: Women who give birth at younger ages (e.g. teenage mothers) are more likely to have children who exhibit behaviour problems, such as attention-deficit/hyperactivity disorder (ADHD). However, it is not clear whether young maternal age is causally associated with poor offspring outcomes or confounded by familial factors.

    Methods: The association between early maternal age at childbirth and offspring ADHD was studied using data from Swedish national registers. The sample included all children born in Sweden between 1988 and 2003 (N = 1 495 543), including 30 674 children with ADHD. We used sibling- and cousin-comparisons to control for unmeasured genetic and environmental confounding. Further, we used a children-of-siblings model to quantify the genetic and environmental contribution to the association between maternal age and offspring ADHD.

    Results: Maternal age at first birth (MAFB) was associated with offspring ADHD. Teenage childbirth (<20 years) was associated with 78% increased risk of ADHD. The association attenuated in cousin-comparison, suggesting unmeasured familial confounding. The children-of-siblings model indicated that the association between MAFB and ADHD was mainly explained by genetic confounding.

    Conclusions: All children born to mothers who bore their first child early in their reproductive lives were at increased risk of ADHD. The association was mainly explained by genetic factors transmitted from mothers to their offspring that contribute to both age at childbirth and ADHD in offspring. Our results highlight the importance of using family-based designs to understand how early life circumstances affect child development.

  • 29.
    Chen, Qi
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Långström, Niklas
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Rodriguez, Alina
    Department of Social Sciences–Psychology, Mid Sweden University, Östersund, Sweden; Department of Epidemiology and Biostatistics, Imperial College London, London, UK; Medical Research Council Social Genetic Developmental Psychiatry Centre, King’s College London, London, UK.
    Serlachius, Eva
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Maternal pre-pregnancy body mass index and offspring attention deficit hyperactivity disorder: a population-based cohort study using a sibling-comparison design2014In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 43, no 1, p. 83-90Article in journal (Refereed)
    Abstract [en]

    Background: High maternal pre-pregnancy body mass index (BMI) is associated with increased risk of offspring attention deficit hyperactivity disorder (ADHD). However, the role of unmeasured familial confounding for this association remains unclear.

    Methods: We conducted a population-based cohort study via linkage of Swedish national and regional registers to investigate maternal pre-pregnancy BMI (underweight: BMI <18.5; overweight: 25≤ BMI <30; obesity: BMI ≥30) in relation to offspring ADHD. We followed 673 632 individuals born in Sweden between 1992 and 2000, with prospectively collected information on maternal pre-pregnancy BMI, until they received an ADHD diagnosis or ADHD medication, death, emigration or 31 December 2009. Hazard ratios (HRs) were estimated by Cox proportional hazards models. Stratified Cox proportional hazards models were applied to data on full siblings to control for unmeasured familial confounding.

    Results: At the population level, pre-pregnancy overweight/obesity was associated with increased risk of offspring ADHD (HR(overweight) = 1.23, 95% CI = 1.18-1.27, P = 0.01; HR(obesity) = 1.64, 95% CI = 1.57-1.73, P = 0.01), after adjustment for measured covariates. In full sibling comparisons, however, previously observed associations no longer remained (HR(overweight) = 0.98, 95% CI = 0.83-1.16, P = 0.82; HR(obesity) = 1.15, 95% CI = 0.85-1.56, P = 0.38).

    Conclusions: The results suggested that the association between maternal pre-pregnancy overweight/obesity and offspring ADHD could be ascribed to unmeasured familial confounding.

  • 30.
    Chen, Qi
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Långström, Niklas
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Rodriguez, Alina
    Mid Sweden University, Faculty of Human Sciences, Department of Psychology. Department of Epidemiology and Biostatistics, Imperial College London, London, United Kingdom .
    Serlachius, Eva
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden .
    D'Onofrio, Brian M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, United States .
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Maternal pre-pregnancy body mass index and offspring attention deficit hyperactivity disorder: a population-based cohort study using a sibling-comparison design2014In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 43, no 1, p. 83-90Article in journal (Refereed)
    Abstract [en]

    Methods We conducted a population-based cohort study via linkage of Swedish national and regional registers to investigate maternal pre-pregnancy BMI (underweight: BMI < 18.5; overweight: 25 BMI < 30; obesity: BMI epsilon 30) in relation to offspring ADHD. We followed 673 632 individuals born in Sweden between 1992 and 2000, with prospectively collected information on maternal pre-pregnancy BMI, until they received an ADHD diagnosis or ADHD medication, death, emigration or 31 December 2009. Hazard ratios (HRs) were estimated by Cox proportional hazards models. Stratified Cox proportional hazards models were applied to data on full siblings to control for unmeasured familial confounding. Results At the population level, pre-pregnancy overweight/obesity was associated with increased risk of offspring ADHD (HRoverweight = 1.23, 95% CI = 1.18-1.27, P = 0.01; HRobesity = 1.64, 95% CI = 1.57-1.73, P = 0.01), after adjustment for measured covariates. In full sibling comparisons, however, previously observed associations no longer remained (HRoverweight = 0.98, 95% CI = 0.83-1.16, P = 0.82; HRobesity = 1.15, 95% CI = 0.85-1.56, P = 0.38). Conclusions The results suggested that the association between maternal pre-pregnancy overweight/obesity and offspring ADHD could be ascribed to unmeasured familial confounding.

  • 31.
    Christian, Parul
    et al.
    Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
    Lee, Sun Eun
    Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
    Donahue Angel, Moira
    Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
    Adair, Linda S
    Department of Nutrition, University of North Carolina, Chapel Hill, NC, USA.
    Arifeen, Shams E
    International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh.
    Ashorn, Per
    Department of International Health, University of Tampere, School of Medicine, Finland.
    Barros, Fernando C
    Programa de Pós-graduação em Saúde e Comportamento, Universidade Católica de Pelotas, Brazil.
    Fall, Caroline Hd
    MRC Lifecourse Epidemiology Unit, Southampton General Hospital, UK.
    Fawzi, Wafaie W
    Departments of Global Health and Population, Nutrition, and Epidemiology, Harvard School of Public Health, Boston, MA, USA.
    Hao, Wei
    Hubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
    Hu, Gang
    Pennington Biomedical Research Center, Baton Rouge, LA, USA.
    Humphrey, Jean H
    Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
    Huybregts, Lieven
    Woman and Child Health Research Center, Department of Public Health, Institute of Tropical Medicine, Antwerpen, Belgium.
    Joglekar, Charu V
    Diabetes Unit, King Edward Memorial Hospital and Research Centre, Pune, India.
    Kariuki, Simon K
    Center for Global Health Research, KEMRI, Kisumu, Kenya.
    Kolsteren, Patrick
    Woman and Child Health Research Center, Department of Public Health, Institute of Tropical Medicine, Antwerpen, Belgium.
    Krishnaveni, Ghattu V
    Epidemiology Research Unit, CSI Holdsworth Memorial Hospital, Mysore, India.
    Liu, Enqing
    Tianjin Women‘s and Children‘s Health Center, Tianjin, China.
    Martorell, Reynaldo
    Hubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
    Osrin, David
    Institute for Global Health, UCL Institute of Child Health, London, UK.
    Persson, Lars-Åke
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Ramakrishnan, Usha
    Hubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
    Richter, Linda
    Human Sciences Research Council and the Developmental Pathways for Health Research Programme, University of the Witwatersrand, Johannesburg, South Africa.
    Roberfroid, Dominique
    Woman and Child Health Research Center, Department of Public Health, Institute of Tropical Medicine, Antwerpen, Belgium.
    Sania, Ayesha
    Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
    Ter Kuile, Feiko O
    KEMRI/CDC Research and Public Health Collaboration, Kisumu, Kenya.
    Tielsch, James
    Department of Global Health, George Washington University, School of Public Health and Health Services, Washington, DC, USA.
    Victora, Cesar G
    Programa de Pós-graduação em Epidemiologia, Universidade Federal de Pelotas, Brazil.
    Yajnik, Chittaranjan S
    Diabetes Unit, King Edward Memorial Hospital and Research Centre, Pune, India.
    Yan, Hong
    Department of Public Health, Xi’an Jiaotong University College of Medicine, Shaanxi, China.
    Zeng, Lingxia
    Department of Public Health, Xi’an Jiaotong University College of Medicine, Shaanxi, China.
    Black, Robert E
    Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
    Risk of childhood undernutrition related to small-for-gestational age and preterm birth in low- and middle-income countries2013In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 42, no 5, p. 1340-1355Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Low- and middle-income countries continue to experience a large burden of stunting; 148 million children were estimated to be stunted, around 30-40% of all children in 2011. In many of these countries, foetal growth restriction (FGR) is common, as is subsequent growth faltering in the first 2 years. Although there is agreement that stunting involves both prenatal and postnatal growth failure, the extent to which FGR contributes to stunting and other indicators of nutritional status is uncertain.

    METHODS:

    Using extant longitudinal birth cohorts (n = 19) with data on birthweight, gestational age and child anthropometry (12-60 months), we estimated study-specific and pooled risk estimates of stunting, wasting and underweight by small-for-gestational age (SGA) and preterm birth.

    RESULTS:

    We grouped children according to four combinations of SGA and gestational age: adequate size-for-gestational age (AGA) and preterm; SGA and term; SGA and preterm; and AGA and term (the reference group). Relative to AGA and term, the OR (95% confidence interval) for stunting associated with AGA and preterm, SGA and term, and SGA and preterm was 1.93 (1.71, 2.18), 2.43 (2.22, 2.66) and 4.51 (3.42, 5.93), respectively. A similar magnitude of risk was also observed for wasting and underweight. Low birthweight was associated with 2.5-3.5-fold higher odds of wasting, stunting and underweight. The population attributable risk for overall SGA for outcomes of childhood stunting and wasting was 20% and 30%, respectively.

    CONCLUSIONS:

    This analysis estimates that childhood undernutrition may have its origins in the foetal period, suggesting a need to intervene early, ideally during pregnancy, with interventions known to reduce FGR and preterm birth.

  • 32.
    Class, Quetzal A.
    et al.
    Department of Obstetrics and Gynecology, University of Illinois, Chicago IL, USA.
    Rickert, Martin E.
    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.
    Öberg, Anna Sara
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston MA, USA.
    Sujan, Ayesha C.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington IN, USA.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Pediatric Allergy and Pulmonology Unit at Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington IN, USA.
    Outcome-dependent associations between short interpregnancy interval and offspring psychological and educational problems: a population-based quasi-experimental study2018In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 47, no 4, p. 1159-1168Article in journal (Refereed)
    Abstract [en]

    Background: Causal interpretation of associations between short interpregnancy interval (the duration from the preceeding birth to the conception of the next-born index child) and the offspring's psychological and educational problems may be influenced by a failure to account for unmeasured confounding.

    Methods: Using population-based Swedish data from 1973-2009, we estimated the association between interpregnancy interval and outcomes [autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), severe mental illness, suicide attempt, criminality, substance-use problem and failing grades] while controlling for measured covariates. We then used cousin comparisons, post-birth intervals (the interval between the second-and third-born siblings to predict second-born outcomes) and sibling comparisons to assess the influence of unmeasured confounding. We included an exploratory analysis of long interpregnancy interval.

    Results: Interpregnancy intervals of 0-5 and 6-11 months were associated with higher odds of outcomes in cohort analyses. Magnitudes of association were attenuated following adjustment for measured covariates. Associations were eliminated for ADHD, severe mental illness and failing grades, but maintained magnitude for ASD, suicide attempt, criminality and substance-use problem in cousin comparisons. Post-birth interpregnancy interval and sibling comparisons suggested some familial confounding. Associations did not persist across models of long interpregnancy interval.

    Conclusions: Attenuation of the association in cousin comparisons and comparable post-birth interval associations suggests that familial genetic or environmental confounding accounts for a majority of the association for ADHD, severe mental illness and failing grades. Modest associations appear independently of covariates for ASD, suicide attempt, criminality and substance-use problem. Post-birth analyses and sibling comparisons, however, show some confounding in these associations.

  • 33.
    Cnattingius, Sven
    et al.
    Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Kramer, Michael S.
    Departments of Pediatrics and of Epidemiology, Biostatistics and Occupational Health, McGill University Faculty of Medicine, Montreal, Canada.
    Norman, Mikael
    Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Stockholm, Sweden; Department of Neonatalogy, Karolinska University Hospital, Stockholm, 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 Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lu, Donghao
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland .
    Keep it in the family: comparing perinatal risks in small-for-gestational-age infants based on population vs within-sibling designs2019In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 48, no 1, p. 297-306Article in journal (Refereed)
    Abstract [en]

    Background: Small-for-gestational-age (SGA) birth is commonly used as a proxy for fetal growth restriction, but also includes constitutionally small infants. Genetic factors account for almost half of the risk of SGA birth. We estimated perinatal risks of SGA birth using both population-based and within-sibling analyses, where the latter by design controls for shared genetic factors and maternal environmental factors that are constant across pregnancies.

    Methods: This was a prospective nationwide cohort study of 2 616 974 singleton infants born in Sweden between January 1987 and December 2012, of whom 1 885 924 were full siblings. We estimated associations between severe or moderate SGA (<3rd percentile and 3rd to <10th percentiles, respectively) and risks of stillbirth, neonatal mortality and morbidity, using both population-based and within-sibling analyses. Hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated in stillbirth analyses, whereas relative risks (RRs) were used for analyses of neonatal outcomes.

    Results: Compared with non-SGA births (>10th percentile), the HR (95% CI) of stillbirth was 18.5 (95% CI 17.4-19.5) among severe SGA births in the population analysis and 22.5 (95% CI 18.7-27.1) in the within-sibling analysis. In non-malformed infants, RRs for neonatal mortality in moderate and severe SGA infants were similarly increased in both population and within-sibling analyses. In term non-malformed infants (>= 37 weeks), SGA-related RRs of several neonatal morbidities were higher in within-sibling than in population analyses.

    Conclusions: Perinatal risks associated with fetal growth restriction are more accurately estimated from analyses of SGA in which genetic factors are accounted for.

  • 34.
    Costa, D.
    et al.
    Univ Porto, P-4100 Oporto, Portugal..
    Hatzidimitriadou, E.
    Univ Kingston, London, England.
    Ioannidi-Kapolou, E.
    Natl Sch Publ Hlth, Athens, Greece..
    Lindert, J.
    Univ Emden, Emden, Germany.
    Soares, Joaquim
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Mid Sweden Univ, Sundsvall, Sweden..
    Sundin, Örjan
    Mid Sweden University, Faculty of Human Sciences, Department of Psychology. Mid Sweden Univ, Ostersund, Sweden..
    Toth, O.
    Hungarian Acad Sci, Budapest, Hungary..
    Barros, H.
    Univ Porto, Inst Publ Hlth, P-4100 Oporto, Portugal..
    Physical Intimate Partner Violence in Europe: Results from a Population-Based Multi-Center Study in Six Countries.2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, no S1, p. 264-264, article id 3583Article in journal (Other academic)
  • 35. Crump, Casey
    et al.
    Friberg, Danielle
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Li, Xinjun
    Sundquist, Jan
    Sundquist, Kristina
    Preterm birth and risk of sleep-disordered breathing from childhood into mid-adulthood.2019In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, article id dyz075Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Preterm birth (gestational age <37 weeks) has previously been associated with cardiometabolic and neuropsychiatric disorders into adulthood, but has seldom been examined in relation to sleep disorders. We conducted the first population-based study of preterm birth in relation to sleep-disordered breathing (SDB) from childhood into mid-adulthood.

    METHODS: A national cohort study was conducted of all 4 186 615 singleton live births in Sweden during 1973-2014, who were followed for SDB ascertained from nationwide inpatient and outpatient diagnoses through 2015 (maximum age 43 years). Cox regression was used to examine gestational age at birth in relation to SDB while adjusting for other perinatal and maternal factors, and co-sibling analyses assessed for potential confounding by unmeasured shared familial factors.

    RESULTS: There were 171 100 (4.1%) persons diagnosed with SDB in 86.0 million person-years of follow-up. Preterm birth was associated with increased risk of SDB from childhood into mid-adulthood, relative to full-term birth (39-41 weeks) [adjusted hazard ratio (aHR), ages 0-43 years: 1.43; 95% confidence interval (CI), 1.40, 1.46; P <0.001; ages 30-43 years: 1.40; 95% CI, 1.34, 1.47; P <0.001]. Persons born extremely preterm (<28 weeks) had more than 2-fold risks (aHR, ages 0-43 years: 2.63; 95% CI, 2.41, 2.87; P <0.001; ages 30-43 years: 2.22; 95% CI, 1.64, 3.01; P <0.001). These associations affected both males and females, but accounted for more SDB cases among males (additive interaction, P = 0.003). Co-sibling analyses suggested that these findings were only partly due to shared genetic or environmental factors in families.

    CONCLUSIONS: Preterm-born children and adults need long-term follow-up for anticipatory screening and potential treatment of SDB.

  • 36. Cutts, F
    et al.
    Dos Santos, C
    Novoa, A
    David, P
    Macassa, Gloria
    Soares, AC
    Child and Maternal Mortality during a Period of Conflict in Beira City, Mozambique1996In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, no 25, p. 349-356Article in journal (Refereed)
  • 37.
    Cutts, F T
    et al.
    London School of Hygiene and Tropical Medicine Keppel St.
    Dos Santos, C
    Ministry of Health Mozambique.
    Novoa, A
    Eduardo Mondlane Faculty of Medicine Mozambique.
    David, P
    London School of Hygiene and Tropical Medicine Keppel St.
    Macassa, Gloria
    Eduardo Mondlane Faculty of Medicine Mozambique.
    Soares, A C
    Eduardo Mondlane Faculty of Medicine Mozambique.
    Child and Maternal Mortality during a Period of Conflict in Beira City, Mozambique1996In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 25, no 2, p. 349-356Article in journal (Refereed)
    Abstract [en]

    Background Child mortality rates have been declining in most developing countries. We studied child and maternal mortality and risk factors for child mortality in Beira city in July 1993, after a decade of conflict in Mozambique.       

    Methods A community-based cluster sample survey of 4609 women of childbearing age was conducted. Indirect techniques were used to estimate child mortality (‘children ever born’ method and Preceding Birth Techniques [PBT]), and maternal mortality sisterhood method). Deaths among the most recent born child, born since July 1990, were classified as cases (n = 106), and two controls, matched by age and cluster, were selected per case.                 

    Results Indirect estimates of the probability of dying from birth to age 5 (deaths before age 5 years, 5q0 per 1000) decreased from 246 in 1977/8 to 212 in 1988/9. The PBT estimate for 1990/91 was 154 (95% confidence interval(CI): 124–184), but recent deaths may have been underreported. Lack of beds in the household (odds ratio[OR] = 2.0, 95% CI: 1.1–3.8), absence of the father (OR = 2.4, 95% CI: 1.2–4.8), low paternal educational level (OR = 2.1, 95% CI: 0.8–5.4), young maternal age (OR = 2.0, 95% CI: 1.0–3.7), self-reported maternal illness (OR = 2.4, 95% CI: 1.2–4.9), and home delivery of the child (OR = 2.3, 95% CI: 1.2–4.5) were associated with increased mortality, but the sensitivity of risk factors was low. Estimated maternal mortality was 410/100 000 live births with a reference date of 1982.                 

    Conclusions Child mortality decreased slowly over the 1980s in Beira despite poor living conditions caused by the indirect effects of the war. Coverage of health services increased over this period. The appropriateness of a risk approach to maternal-child-health care needs further evaluation.

  • 38. Dekhtyar, Serhiy
    et al.
    Wang, Hui-Xin
    Stockholm University, Faculty of Social Sciences, Aging Research Center (ARC), (together with KI). Zhengzhou University, China.
    Fratiglioni, Laura
    Stockholm University, Faculty of Social Sciences, Aging Research Center (ARC), (together with KI).
    Herlitz, Agneta
    Childhood school performance, education and occupational complexity: a life-course study of dementia in the Kungsholmen Project2016In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 45, no 4, p. 1207-1215Article in journal (Refereed)
    Abstract [en]

    Background: Cognitive reserve hypothesis predicts that intellectually demanding activities over the life course protect against dementia. We investigate if childhood school performance remains associated with dementia once education and occupational complexity are taken into account. Methods: A cohort of 440 individuals aged 75+ from the Kungsholmen Project was followed up for 9 years to detect dementia. To measure early-life contributors to reserve, we used grades at age 9-10 extracted from the school archives. Data on formal education and occupational complexity were collected at baseline and first follow-up. Dementia was ascertained through comprehensive clinical examination. Cox models estimated the relationship between life-course cognitive reserve measures and dementia. Results: Dementia risk was elevated [hazard ratio (HR): 1.54, 95% confidence interval (CI): 1.03 to 2.29] in individuals with low early-life school grades after adjustment for formal educational attainment and occupational complexity. Secondary education was associated with a lower risk of dementia (HR: 0.72, 95% CI: 0.50 to 1.03), although the effects of post-secondary and university degrees were indistinguishable from baseline. Occupational complexity with data and things was not related to dementia. However, an association was found between high occupational complexity with people and dementia, albeit only in women (HR: 0.39, 95% CI: 0.14 to 0.99). The pattern of results remained unchanged after adjustment for genetic susceptibility, comorbidities and depressive symptoms. Conclusion: Low early-life school performance is associated with an elevated risk of dementia, independent of subsequent educational and occupational attainment.

  • 39.
    Desvars, Amélie
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology.
    Furberg, Maria
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Hjertqvist, Marika
    Vidman, Linda
    Umeå University, Faculty of Science and Technology, Department of Mathematics and Mathematical Statistics.
    Sjöstedt, Anders
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology.
    Rydén, Patrik
    Umeå University, Faculty of Science and Technology, Department of Mathematics and Mathematical Statistics.
    Johansson, Anders
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology.
    Epidemiology and Ecology of Tularemia in Sweden2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, p. 58-58Article in journal (Other academic)
  • 40. Diderichsen, F
    et al.
    Hallqvist, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy.
    Trends in occupational mortality among middle-aged men in Sweden 1961-1990.1997In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 26, no 4, p. 782-7Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Many European countries have in recent decades reported growing socioeconomic differentials in mortality. While these trends have usually paralleled high unemployment and increasing income disparities, Sweden had low unemployment and narrowing income differences. This study describes trends, 1961-1990, in total and cardiovascular mortality among men, 45-69 years of age, in major occupational classes in Sweden.

    METHODS: From census data four cohorts were created from those enumerated in 1960, 1970, 1980 and 1985. Through record linkage with the Swedish cause of death registry the mortality in each cohort was followed for 5-10 years. Age-standardized mortality trends 1961-1990 were calculated for occupational groups, categorized according to sector of the economy.

    RESULTS: The increase in mortality among middle-aged men in Sweden 1965-1980 was mainly a result of increasing cardiovascular mortality among industrial workers and farmers. In the 1980s the trend for these groups changed into a last decrease in mortality similar to that for non-manual occupations for the whole period. Consequently the rate ratio for industrial workers in comparison with men having a professional/managerial type of occupation increased from 0.98 to 1.43. The slowest decrease is now found among unqualified occupations in services and transportation.

    CONCLUSIONS: While Sweden, during the period studied, had narrowing income differentials and low unemployment this result points to the importance of working conditions in understanding trends and distribution of male adult mortality.

  • 41.
    Diderichsen, Finn
    et al.
    Univ Copenhagen, Dept Publ Hlth, Copenhagen, Denmark; Fundacao Oswaldo Cruz, Dept Saude Colet, Recife, PE, Brazil.
    Hallqvist, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine.
    Whitehead, Margaret
    Univ Liverpool, Dept Publ Hlth & Policy, Liverpool, Merseyside, England.
    Differential vulnerability and susceptibility: how to make use of recent development in our understanding of mediation and interaction to tackle health inequalities2019In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 48, no 1, p. 268-274Article in journal (Refereed)
    Abstract [en]

    This paper discusses the concepts of vulnerability and susceptibility and their relevance for understanding and tackling health inequalities. Tackling socioeconomic inequalities in health is based on an understanding of how an individual's social position influences disease risk. Conceptually, there are two possible mechanisms (not mutually exclusive): there is either some cause(s) of disease that are unevenly distributed across socioeconomic groups (differential exposure) or the effect of some cause(s) of disease differs across groups (differential effect). Since differential vulnerability and susceptibility are often used to denote the latter, we discuss these concepts and their current use and suggest an epidemiologically relevant distinction. The effect of social position can thus be mediated by causes that are unevenly distributed across social groups and/or interact with social position. Recent improvements in the methodology to estimate mediation and interaction have made it possible to calculate measures of relevance for setting targets and priorities in policy for health equity which include both mechanisms, i.e. equalize exposure or equalize effects. We finally discuss the importance of differential susceptibility and vulnerability for the choice of preventive strategies, including approaches that target high-risk individuals, whole populations and vulnerable groups.

  • 42.
    du Prel, J. B.
    et al.
    Univ Ulm, Inst Hist Philosophy & Eth Med, D-89069 Ulm, Germany..
    Runeson-Broberg, R.
    Univ Uppsala Hosp, Occupat & Environm Med, Uppsala, Sweden..
    Westerholm, P.
    Univ Uppsala Hosp, Occupat & Environm Med, Uppsala, Sweden..
    Nordin, M.
    Stockholm Univ, Stress Res Inst, S-10691 Stockholm, Sweden..
    Fahlen, G.
    Natl Agcy Special Needs Educ & Sch, Harnosand, Sweden..
    Alfredsson, L.
    Karolinska Inst, Stockholm, Sweden..
    Knutsson, Anders
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Mid Sweden Univ, Sundsvall, Sweden..
    Peter, R.
    Univ Ulm, Inst Hist Philosophy & Eth Med, D-89069 Ulm, Germany..
    Work-Related Overcommitment: Is it a State or a Trait? - Results from the Swedish WOLF-Study.2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, no S1, p. 263-263, article id 3649Article in journal (Other academic)
  • 43.
    du Prel, J. B.
    et al.
    Univ Ulm, Inst Hist Philosophy & Eth Med, D-89069 Ulm, Germany..
    Runeson-Broberg, Roma
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Westerholm, Peter
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Nordin, M.
    Stockholm Univ, Stress Res Inst, S-10691 Stockholm, Sweden..
    Fahlen, G.
    Natl Agcy Special Needs Educ & Sch, Harnosand, Sweden..
    Alfredsson, L.
    Karolinska Inst, Stockholm, Sweden..
    Knutsson, A.
    Mid Sweden Univ, Sundsvall, Sweden..
    Peter, R.
    Univ Ulm, Inst Hist Philosophy & Eth Med, D-89069 Ulm, Germany..
    Work-Related Overcommitment: Is it a State or a Trait? - Results from the Swedish WOLF-Study2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, p. 263-263Article in journal (Other academic)
  • 44.
    Edvardsson, Kristina
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology. Judith Lumley Centre, La Trobe University, Bundoora, VIC, Australia.
    Axmon, Anna
    Powell, Rhonda
    Davey, Mary-Ann
    Male-biased sex ratios in Australian migrant populations: a population-based study of 1 191 250 births 1999-20152018In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 47, no 6, p. 2025-2037Article in journal (Refereed)
    Abstract [en]

    Background: The naturally occurring male-to-female (M/F) ratio at birth is 1.05. Higher ratios found primarily in countries across Asia have been attributed to prenatal sex selection due to son preference. There is growing evidence that sex-selective practices continue following migration; however, little is known about these practices following migration to Australia.

    Methods: In this population-based study we assessed M/F ratios at birth per mother’s country of birth for all registered births 1999–2015 in Victoria, Australia (n = 1 191 250). We also compared the M/F ratio among births to mothers born elsewhere to that of mothers born in Australia, stratified by time period and parity.

    Results: Compared with the naturally occurring M/F ratio as well as to the M/F ratio among births to mothers born in Australia, there was an increased ratio of male births to mothers born in India, China and South-East Asia, particularly at higher parities and in more recent time periods (elevated M/F ratios ranged from 1·079 to 1·248, relative risks of male birth ranged from 1·012 to 1·084 with confidence intervals between 1·001 and 1·160 and P-values between 0·005 and 0·039). The most male-biased sex ratios were found among multiple births to Indian-born mothers, and parity of two or more births to Indian and Chinese-born mothers in 2011–15.

    Conclusions: The male-biased sex ratios observed in this study indicate that prenatal sex selection may be continuing following migration to Australia from countries where these practices have been documented. The excess of males among multiple births raises the question as to what role assisted reproduction plays. Findings also suggest that systematic discrimination against females starts in the womb.

  • 45.
    Ekström, Eva-Charlotte
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Lindström, Emma
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Raqib, Rubhana
    El Arifeen, Shams
    Basu, Samar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Oxidative Stress and Inflammation.
    Brismar, Kerstin
    Selling, Katarina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Persson, Lars-Åke
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Effects of prenatal micronutrient and early food supplementation on metabolic status of the offspring at 4.5 years of age. The MINIMat randomized trial in rural Bangladesh.2016In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 45, no 5, p. 1656-1667Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Fetal nutritional insults may alter the later metabolic phenotype. We hypothesized that early timing of prenatal food supplementation and multiple micronutrient supplementation (MMS) would favourably influence childhood metabolic phenotype.

    METHODS: Pregnant women recruited 1 January to 31 December 2002 in Matlab, Bangladesh, were randomized into supplementation with capsules of either 30 mg of iron and 400 μg of folic acid, 60 mg of iron and 400 μg of folic acid, or MMS containing a daily allowance of 15 micronutrients, and randomized to food supplementation (608 kcal) either with early invitation (9 weeks' gestation) or usual invitation (at 20 weeks). Their children (n = 1667) were followed up at 4.5 years with assessment of biomarkers of lipid and glucose metabolism, inflammation and oxidative stress.

    RESULTS: Children in the group with early timing of food supplementation had lower cholesterol (difference -0.079 mmol/l, 95% confidence interval (CI) -0.156; -0.003), low-density lipoprotein (LDL) (difference -0.068 mmol/l, 95% CI -0.126; -0.011) and ApoB levels (difference -0.017 g/l, 95% CL -0.033; -0.001). MMS supplementation resulted in lower high-density lipoprotein (HDL) (difference -0.028 mmol/l, 95% CL -0.053; -0.002), lower glucose (difference -0.099 mmol/l, 95% CL -0.179; -0.019) and lower insulin-like growth factor 1 (IGF-1) (difference on log scale -0.141 µg/l, 95% CL -0.254; -0.028) than 60 mg iron and 400 μg folic acid. There were no effects on markers of inflammation or oxidative stress.

    CONCLUSIONS: Findings suggest that in a population where malnutrition is prevalent, nutrition interventions during pregnancy may modify the metabolic phenotype in the young child that could have consequences for later chronic disease risks.

  • 46.
    Emilsson, L.
    et al.
    Primary Care Res Unit, Varmlands Nysater, Sweden..
    Lindahl, Bertil
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Koster, M.
    Natl Board Hlth & Welf, Stockholm, Sweden..
    Lambe, M.
    Karolinska Inst, Stockholm, Sweden..
    Ludvigsson, J. F.
    Karolinska Inst, Stockholm, Sweden..
    Review of 103 Swedish Healthcare Quality Registers2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, p. 174-174Article in journal (Other academic)
  • 47.
    Ericsson, Malin
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Pedersen, Nancy L.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Johansson, Anna L. V.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fors, Stefan
    Aging Research Center, Karolinska Institutet.
    Dahl Aslan, Anna K.
    Jönköping University, School of Health and Welfare, HHJ, Institute of Gerontology. Jönköping University, School of Health and Welfare, HHJ. ARN-J (Aging Research Network - Jönköping). Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Life-course socioeconomic differences and social mobility in preventable and non-preventable mortality: a study of Swedish twins2019In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Despite advances in life expectancy, low socioeconomic status is associated with a shorter lifespan. This study was conducted to investigate socioeconomic differences in mortality by comparing preventable with non-preventable causes of death in 39 506 participants from the Swedish Twin Registry born before 1935.

    METHODS: Childhood social class, own education, own social class and social mobility were used as separate indicators of socioeconomic status. These data were linked to the Swedish Cause of Death Register. Cause of death was categorized as preventable or non-preventable mortality according to indicators presented in the Avoidable Mortality in the European Union (AMIEHS) atlas. Using Cox proportional hazard models, we tested the association between the socioeconomic measures and all-cause mortality, preventable mortality and non-preventable mortality. Additional co-twin control analyses indicated whether the associations reflected genetic confounding.

    RESULTS: The social gradient for mortality was most prominent for the adult socioeconomic measures. There was a social gradient in both preventable mortality and non-preventable mortality, but with an indication of a moderately stronger effect in preventable causes of death. In analyses of social mobility, those who experienced life-time low socioeconomic status (SES) or downward social mobility had an increased mortality risk compared with those with life-time high SES and upward social mobility. Adjustments for genetic confounding did not change the observed associations for education, social class or social mobility and mortality. In the co-twin control analyses of reared-apart twins, the association between childhood social class and mortality weakened, indicating possible genetic influences on this association.

    CONCLUSIONS: Our results indicate that there is an association between low adult socioeconomic status and increased mortality independent of genetic endowment. Thus, we do not find support for indirect social selection as the basis for mortality inequalities in Sweden.

  • 48. Farahmand, Bahman Y.
    et al.
    Persson, Per-Gunnar
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Baron, John A.
    Alberts, Akke
    Moradi, Tahere
    Ljunghall, Sverker
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Physical activity and hip fracture: a population-based case-control study2000In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 29, no 2, p. 308-14Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: A growing body of literature suggests that physical activity may be a protective factor against hip fracture. METHODS: To study the association between hip fracture risk and recreational physical activity at various ages, changes in activity during adult life, occupational physical activity and how risks vary by adult weight change, we performed a population-based case-control study among postmenopausal women aged 50-81 years residing in six counties in Sweden in 1993-1995. The analysis consisted of 1327 women with hip fracture and 3262 randomly selected controls. Information on leisure physical activity before age 18, at 18-30 years and during recent years was based on a questionnaire. Data on occupational physical activity were collected through an independent classification of job titles obtained from record linkage with census data from 1960, 1970 and 1980. RESULTS: There was a protective effect of recent leisure physical activity. Compared to women who reported no leisure activity, the odds ratios (OR) were 0.79 (95% CI: 0.62-1.00), 0.67 (95% CI: 0.54-0.84) and 0.48 (95% CI: 0.39-0.60) for women who exercised <1 h per week, 1-2 h per week, and 3+ h per week, respectively. These decreased OR were more pronounced in women who had lost weight after 18 years of age than in those who had gained weight. Women with high physical activity at both 18-30 years and during recent years did not have a stronger protection than those with isolated high activity late in life, after accounting for recent activity. Occupational physical activity was not associated with hip fracture risk in this study. CONCLUSIONS: Recent physical activity is protective against hip fracture. The protective effect is most pronounced in women who had lost weight after age 18.

  • 49.
    Forsberg, Bertil
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Environmental Medicine.
    Pekkanen, J
    Clench-Aas, J
    Mårtensson, MB
    Stjernberg, Nils
    Bartonova, A
    Timonen, KL
    Skerfving, S
    Childhood asthma in four regions in Scandinavia: risk factors and avoidance effects1997In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 26, no 3, p. 610-619Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The high and increasing prevalence of childhood asthma is a major public health issue. Various risk factors have been proposed in local studies with different designs.

    METHODS: We have made a questionnaire study of the prevalence of childhood asthma, potential risk factors and their relations in four regions in Scandinavia (Umeå and Malmö in Sweden, Kuopio in eastern Finland and Oslo, Norway). One urban and one less urbanized area were selected in each region, and a study group of 15962 children aged 6-12 years was recruited.

    RESULTS: The prevalence of symptoms suggestive of asthma varied considerably between different areas (dry cough 8-19%, asthma attacks 4-8%, physician-diagnosed asthma 4-9%), as did the potential risk factors. Urban residency was generally not a risk factor. However, dry cough was common in the most traffic polluted area. Exposure to some of the risk factors. such as smoking indoors and moisture stains or moulds at home during the first 2 years of life, resulted in an increased risk. However, current exposure was associated with odds ratios less than one.

    CONCLUSIONS: Our findings were probably due to a combination of early impact and later avoidance of these risk factors. The effects of some risk factors were found to differ significantly between regions. No overall pattern between air pollution and asthma was seen, but air pollution differed less than expected between the areas.

  • 50.
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Skane Univ Hosp, Dept Clin Sci, Malmo, Sweden ; Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
    Commentary: mining gene-lifestyle interactions in UK Biobank: all that glitters isn't gold2017In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 46, no 2, p. 576-577Article in journal (Refereed)
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