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  • 1. Andrae, Bengt
    et al.
    Andersson, Therese M-L
    Lambert, Paul C
    Kemetli, Levent
    Silfverdal, Lena
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Obstetrik och gynekologi.
    Strander, Björn
    Ryd, Walter
    Dillner, Joakim
    Törnberg, Sven
    Sparén, Pär
    Screening and cervical cancer cure: population based cohort study2012Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 344, s. e900-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective To determine whether detection of invasive cervical cancer by screening results in better prognosis or merely increases the lead time until death.

    Design Nationwide population based cohort study. Setting Sweden.

    Participants All 1230 women with cervical cancer diagnosed during 1999-2001 in Sweden prospectively followed up for an average of 8.5 years. Main outcome measures Cure proportions and five year relative survival ratios, stratified by screening history, mode of detection, age, histopathological type, and FIGO (International Federation of Gynecology and Obstetrics) stage.

    Results In the screening ages, the cure proportion for women with screen detected invasive cancer was 92% (95% confidence interval 75% to 98%) and for symptomatic women was 66% (62% to 70%), a statistically significant difference in cure of 26% (16% to 36%). Among symptomatic women, the cure proportion was significantly higher for those who had been screened according to recommendations (interval cancers) than among those overdue for screening: difference in cure 14% (95% confidence interval 6% to 23%). Cure proportions were similar for all histopathological types except small cell carcinomas and were closely related to FIGO stage. A significantly higher cure proportion for screen detected cancers remained after adjustment for stage at diagnosis (difference 15%, 7% to 22%).

    Conclusions Screening is associated with improved cure of cervical cancer. Confounding cannot be ruled out, but the effect was not attributable to lead time bias and was larger than what is reflected by down-staging. Evaluations of screening programmes should consider the assessment of cure proportions.

  • 2.
    Blomstedt, Yulia
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa.
    Bhutta, Zulfiqar A.
    Dahlstrand, Johan
    Friberg, Peter
    Gostin, Lawrence O.
    Nilsson, Måns
    Sewankambo, Nelson K.
    Tomson, Göran
    Alfvén, Tobias
    Partnerships for child health: capitalising on links between the sustainable development goals2018Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 360, artikkel-id k125Artikkel i tidsskrift (Annet vitenskapelig)
  • 3.
    Brunström, Mattias
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Carlberg, Bo
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Effect of antihypertensive treatment at different blood pressure levels in patients with diabetes mellitus: systematic review and meta-analyses2016Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 352, artikkel-id i717Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Objective: To assess the effect of antihypertensive treatment on mortality and cardiovascular morbidity in people with diabetes mellitus, at different blood pressure levels.

    Design: Systematic review and meta-analyses of randomised controlled trials.

    Data sources: CENTRAL, Medline, Embase, and BIOSIS were searched using highly sensitive search strategies. When data required according to the protocol were missing but trials were potentially eligible, we contacted researchers, pharmaceutical companies, and authorities.

    Eligibility criteria: Randomised controlled trials including 100 or more people with diabetes mellitus, treated for 12 months or more, comparing any antihypertensive agent against placebo, two agents against one, or different blood pressure targets.

    Results: 49 trials, including 73 738 participants, were included in the meta-analyses. Most of the participants had type 2 diabetes. If baseline systolic blood pressure was greater than 150 mm Hg, antihypertensive treatment reduced the risk of all cause mortality (relative risk 0.89, 95% confidence interval 0.80 to 0.99), cardiovascular mortality (0.75, 0.57 to 0.99), myocardial infarction (0.74, 0.63 to 0.87), stroke (0.77, 0.65 to 0.91), and end stage renal disease (0.82, 0.71 to 0.94). If baseline systolic blood pressure was 140-150 mm Hg, additional treatment reduced the risk of all cause mortality (0.87, 0.78 to 0.98), myocardial infarction (0.84, 0.76 to 0.93), and heart failure (0.80, 0.66 to 0.97). If baseline systolic blood pressure was less than 140 mm Hg, however, further treatment increased the risk of cardiovascular mortality (1.15, 1.00 to 1.32), with a tendency towards an increased risk of all cause mortality (1.05, 0.95 to 1.16). Metaregression analyses showed a worse treatment effect with lower baseline systolic blood pressures for cardiovascular mortality (1.15, 1.03 to 1.29 for each 10 mm Hg lower systolic blood pressure) and myocardial infarction (1.12, 1.03 to 1.22 for each 10 mm Hg lower systolic blood pressure). Patterns were similar for attained systolic blood pressure.

    Conclusions: Antihypertensive treatment reduces the risk of mortality and cardiovascular morbidity in people with diabetes mellitus and a systolic blood pressure more than 140 mm Hg. If systolic blood pressure is less than 140 mm Hg, however, further treatment is associated with an increased risk of cardiovascular death, with no observed benefit.

  • 4. Ding, Ming
    et al.
    Huang, Tao
    Bergholdt, Helle K. M.
    Nordestgaard, Borge G.
    Ellervik, Christina
    Qi, Lu
    Frazier-Wood, Alexis C.
    Aslibekyan, Stella
    North, Kari E.
    Voortman, Trudy
    Graff, Mariaelisa
    Smith, Caren E.
    Lai, Chao-Qiang
    Varbo, Anette
    Lemaitre, Rozenn N.
    de Jonge, Ester A. L.
    Fumeron, Frederic
    Corella, Dolores
    Wang, Carol A.
    Tjonneland, Anne
    Overvad, Kim
    Sorensen, Thorkild I. A.
    Feitosa, Mary F.
    Wojczynski, Mary K.
    Kahonen, Mika
    Ahmad, Shafqat
    Renström, Frida
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning. Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Psaty, Bruce M.
    Siscovick, David S.
    Barroso, Ines
    Johansson, Ingegerd
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning.
    Hernandez, Dena
    Ferrucci, Luigi
    Bandinelli, Stefania
    Linneberg, Allan
    Sandholt, Camilla Helene
    Pedersen, Oluf
    Hansen, Torben
    Schulz, Christina-Alexandra
    Sonestedt, Emily
    Orho-Melander, Marju
    Chen, Tzu-An
    Rotter, Jerome I.
    Allison, Mathew A.
    Rich, Stephen S.
    Sorli, Jose V.
    Coltell, Oscar
    Pennell, Craig E.
    Eastwood, Peter R.
    Hofman, Albert
    Uitterlinden, Andre G.
    Zillikens, MCarola
    van Rooij, Frank J. A.
    Chu, Audrey Y.
    Rose, Lynda M.
    Ridker, Paul M.
    Viikari, Jorma
    Raitakari, Olli
    Lehtimaki, Terho
    Mikkila, Vera
    Willett, Walter C.
    Wang, Yujie
    Tucker, Katherine L.
    Ordovas, Jose M.
    Kilpelainen, Tuomas O.
    Province, Michael A.
    Franks, Paul W.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin. Department of Nutrition, Harvard School of Public Health, Boston, MA 02115, USA; Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Arnett, Donna K.
    Tanaka, Toshiko
    Toft, Ulla
    Ericso, Ulrika
    Franco, Oscar H.
    Mozaffarian, Dariush
    Hu, Frank B.
    Chasman, Daniel I.
    Dairy consumption, systolic blood pressure, and risk of hypertension: Mendelian randomization study2017Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 356, artikkel-id j1000Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE To examine whether previous observed inverse associations of dairy intake with systolic blood pressure and risk of hypertension were causal. DESIGN Mendelian randomization study using the single nucleotide polymorphism rs4988235 related to lactase persistence as an instrumental variable. SETTING CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) Consortium. PARTICIPANTS Data from 22 studies with 171 213 participants, and an additional 10 published prospective studies with 26 119 participants included in the observational analysis. MAIN OUTCOME MEASURES The instrumental variable estimation was conducted using the ratio of coefficients approach. Using metaanalysis, an additional eight published randomized clinical trials on the association of dairy consumption with systolic blood pressure were summarized. RESULTS Compared with the CC genotype (CC is associated with complete lactase deficiency), the CT/TT genotype (TT is associated with lactose persistence, and CT is associated with certain lactase deficiency) of LCT-13910 (lactase persistence gene) rs4988235 was associated with higher dairy consumption (0.23 (about 55 g/day), 95% confidence interval 0.17 to 0.29) serving/day; P<0.001) and was not associated with systolic blood pressure (0.31, 95% confidence interval -0.05 to 0.68 mm Hg; P=0.09) or risk of hypertension (odds ratio 1.01, 95% confidence interval 0.97 to 1.05; P=0.27). Using LCT-13910 rs4988235 as the instrumental variable, genetically determined dairy consumption was not associated with systolic blood pressure (beta=1.35, 95% confidence interval -0.28 to 2.97 mm Hg for each serving/day) or risk of hypertension (odds ratio 1.04, 0.88 to 1.24). Moreover, meta-analysis of the published clinical trials showed that higher dairy intake has no significant effect on change in systolic blood pressure for interventions over one month to 12 months (intervention compared with control groups: beta=-0.21, 95% confidence interval -0.98 to 0.57 mm Hg). In observational analysis, each serving/day increase in dairy consumption was associated with -0.11 (95% confidence interval -0.20 to -0.02 mm Hg; P=0.02) lower systolic blood pressure but not risk of hypertension (odds ratio 0.98, 0.97 to 1.00; P=0.11). CONCLUSION The weak inverse association between dairy intake and systolic blood pressure in observational studies was not supported by a comprehensive instrumental variable analysis and systematic review of existing clinical trials.

  • 5. Hariz, Marwan I
    et al.
    Hariz, Gun-Marie
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Arbetsterapi.
    Hyping deep brain stimulation in psychiatry could lead to its demise2012Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 345, s. e5447-Artikkel i tidsskrift (Annet vitenskapelig)
  • 6. Heikkila, Katriina
    et al.
    Nyberg, Solja T.
    Theorell, Tores
    Fransson, Eleonor I.
    Alfredsson, Lars
    Bjorner, Jakob B.
    Bonenfant, Sebastien
    Borritz, Marianne
    Bouillon, Kim
    Burr, Herman
    Dragano, Nico
    Geuskens, Goedele A.
    Goldberg, Marcel
    Hamer, Mark
    Hooftman, Wendela E.
    Houtman, Irene L.
    Joensuu, Matti
    Knutsson, Anders
    Koskenvuo, Markku
    Koskinen, Aki
    Kouvonen, Anne
    Madsen, Ida E. H.
    Magnusson, Linda L.
    Marmot, Michael G.
    Nielsen, Martin L.
    Nordin, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Oksanen, Tuula
    Pentti, Jaana
    Salo, Paula
    Rugulies, Reiner
    Steptoe, Andrew
    Suominen, Sakari
    Vahtera, Jussi
    Virtanen, Marianna
    Vaananen, Ari
    Westerholm, Peter
    Westerlund, Hugo
    Zins, Marie
    Ferrie, Jane E.
    Singh-Manoux, Archana
    Batty, G. David
    Kivimaki, Mika
    Work stress and risk of cancer: meta-analysis of 5700 incident cancer events in 116 000 European men and women2013Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 346, s. f165-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective To investigate whether work related stress, measured and defined as job strain, is associated with the overall risk of cancer and the risk of colorectal, lung, breast, or prostate cancers.

    Design Meta-analysis of pooled prospective individual participant data from 12 European cohort studies including 116 056 men and women aged 17-70 who were free from cancer at study baseline and were followed-up for a median of 12 years. Work stress was measured and defined as job strain, which was self reported at baseline. Incident cancers (all n=5765, colorectal cancer n=522, lung cancer n=374, breast cancer n=1010, prostate cancer n=865) were ascertained from cancer, hospital admission, and death registers. Data were analysed in each study with Cox regression and the study specific estimates pooled in meta-analyses. Models were adjusted for age, sex, socioeconomic position, body mass index (BMI), smoking, and alcohol intake

    Results A harmonised measure of work stress, high job strain, was not associated with overall risk of cancer (hazard ratio 0.97, 95% confidence interval 0.90 to 1.04) in the multivariable adjusted analyses. Similarly, no association was observed between job strain and the risk of colorectal (1.16, 0.90 to 1.48), lung (1.17, 0.88 to 1.54), breast (0.97, 0.82 to 1.14), or prostate (0.86, 0.68 to 1.09) cancers. There was no clear evidence for an association between the categories of job strain and the risk of cancer.

    Conclusions These findings suggest that work related stress, measured and defined as job strain, at baseline is unlikely to be an important risk factor for colorectal, lung, breast, or prostate cancers.

  • 7. Kivimaki, Mika
    et al.
    Singh-Manoux, Archana
    Pentti, Jaana
    Sabia, Severine
    Nyberg, Solja T.
    Alfredsson, Lars
    Goldberg, Marcel
    Knutsson, Anders
    Koskenvuo, Markku
    Koskinen, Aki
    Kouvonen, Anne
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Oksanen, Tuula
    Strandberg, Timo
    Suominen, Sakari B.
    Theorell, Tores
    Vahtera, Jussi
    Vaananen, Ari
    Virtanen, Marianna
    Westerholm, Peter
    Westerlund, Hugo
    Zins, Marie
    Seshadri, Sudha
    Batty, G. David
    Sipila, Pyry N.
    Shipley, Martin J.
    Lindbohm, Joni V.
    Ferrie, Jane E.
    Jokela, Markus
    Physical inactivity, cardiometabolic disease, and risk of dementia: an individual-participant meta-analysis2019Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 365, artikkel-id l1495Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE To examine whether physical inactivity is a risk factor for dementia, with attention to the role of cardiometabolic disease in this association and reverse causation bias that arises from changes in physical activity in the preclinical (prodromal) phase of dementia. DESIGN Meta-analysis of 19 prospective observational cohort studies. DATA SOURCES The Individual-Participant-Data Meta-analysis in Working Populations Consortium, the Inter-University Consortium for Political and Social Research, and the UK Data Service, including a total of 19 of a potential 9741 studies. REVIEW METHOD The search strategy was designed to retrieve individual-participant data from prospective cohort studies. Exposure was physical inactivity; primary outcomes were incident all-cause dementia and Alzheimer's disease; and the secondary outcome was incident cardiometabolic disease (that is, diabetes, coronary heart disease, and stroke). Summary estimates were obtained using random effects meta-analysis. RESULTS Study population included 404 840 people (mean age 45.5 years, 57.7% women) who were initially free of dementia, had a measurement of physical inactivity at study entry, and were linked to electronic health records. In 6.0 million person-years at risk, we recorded 2044 incident cases of all-cause dementia. In studies with data on dementia subtype, the number of incident cases of Alzheimer's disease was 1602 in 5.2 million person-years. When measured < 10 years before dementia diagnosis (that is, the preclinical stage of dementia), physical inactivity was associated with increased incidence of all-cause dementia (hazard ratio 1.40, 95% confidence interval 1.23 to 1.71) and Alzheimer's disease (1.36, 1.12 to 1.65). When reverse causation was minimised by assessing physical activity >= 10 years before dementia onset, no difference in dementia risk between physically active and inactive participants was observed (hazard ratios 1.01 (0.89 to 1.14) and 0.96 (0.85 to 1.08) for the two outcomes). Physical inactivity was consistently associated with increased risk of incident diabetes (hazard ratio 1.42, 1.25 to 1.61), coronary heart disease (1.24, 1.13 to 1.36), and stroke (1.16, 1.05 to 1.27). Among people in whom cardiometabolic disease preceded dementia, physical inactivity was non-significantly associated with dementia (hazard ratio for physical activity assessed > 10 before dementia onset 1.30, 0.79 to 2.14). CONCLUSIONS In analyses that addressed bias due to reverse causation, physical inactivity was not associated with all-cause dementia or Alzheimer's disease, although an indication of excess dementia risk was observed in a subgroup of physically inactive individuals who developed cardiometabolic disease.

  • 8. Ludvigsson, Jonas F
    et al.
    Ivarsson, Anneli
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och folkhälsovetenskap.
    Coeliac disease: Decision tool needs to be developed for children.2007Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 334, nr 7599, s. 864-Artikkel i tidsskrift (Annet vitenskapelig)
  • 9.
    Lynöe, Niels
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Socialmedicin.
    Sandlund, Mikael
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Jacobsson, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Informed consent: study of quality of information given to participants in a clinical trial1991Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 303, nr 6803, s. 610-613Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To determine whether the participants in a clinical trial had perceived adequate information about the trial according to the guidelines of the Declaration of Helsinki. DESIGN: About 18 months after the end of a gynaecological clinical trial the participants received a questionnaire by post, which focused on the quality of the information given to them before entering the trial. Neither researchers nor participants were aware in advance that the trial would become the subject of this follow up investigation. SETTING: Eight different centres in Sweden. SUBJECTS: 43 women out of the 53 who completed the trial (mean (range) age 23 (16 to 35) years) returned the questionnaire. MAIN OUTCOME MEASURES: Adequacy of the information (based on requirements of the Declaration of Helsinki) to enable the following: understanding of the aims of the study; awareness of what participation meant; and awareness of the possibility of withdrawing from participation at any time. Motives for agreeing to participate, and a subjective evaluation of the given information were also recorded. RESULTS: All but one of the participants had been aware that they were taking part in a research project. Five women stated that they had not been aware that a second laparoscopy was performed only for research reasons. Seven women reported that they had not been aware of the meaning of participating in the project and 17 that they had had no information about the possibility of withdrawing from the study whenever they wanted. In the subjective rating 22 women considered the information given as good or very good. There was a systematic variation in the quality of the given information among the eight centres. CONCLUSION: Although all but one of the participants had been aware that they were taking part in a clinical trial, the quality of the information understood and recalled by participants varied, and in many cases clearly did not meet the guidelines of the Declaration of Helsinki. Variations among centres in participants' perception of information suggest that deficiencies in perception may be caused by informers rather than the participants.

  • 10. Muller, David C.
    et al.
    Larose, Tricia L.
    Hodge, Allison
    Guida, Florence
    Langhammer, Arnulf
    Grankvist, Kjell
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap.
    Meyer, Klaus
    Cai, Qiuyin
    Arslan, Alan A.
    Zeleniuch-Jacquotte, Anne
    Albanes, Demetrius
    Giles, Graham G.
    Sesso, Howard D.
    Lee, I-Min
    Gaziano, J. Michael
    Yuan, Jian-Min
    Bolton, Judith Hoffman
    Buring, Julie E.
    Visvanathan, Kala
    Le Marchand, Loic
    Purdue, Mark P.
    Caporaso, Neil E.
    Midttun, Oivind
    Ueland, Per M.
    Prentice, Ross L.
    Weinstein, Stephanie J.
    Stevens, Victoria L.
    Zheng, Wei
    Blot, William J.
    Shu, Xiao-Ou
    Zhang, Xuehong
    Xiang, Yong-Bing
    Koh, Woon-Puay
    Hveem, Kristian
    Thomson, Cynthia A.
    Pettinger, Mary
    Engstrom, Gunnar
    Brunnstrom, Hans
    Milne, Roger L.
    Stampfer, Meir J.
    Han, Jiali
    Johansson, Mikael
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
    Brennan, Paul
    Severi, Gianluca
    Johansson, Mattias
    Circulating high sensitivity C reactive protein concentrations and risk of lung cancer: nested case-control study within Lung Cancer Cohort Consortium2019Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 364, artikkel-id k4981Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives To conduct a comprehensive analysis of prospectively measured circulating high sensitivity C reactive protein (hsCRP) concentration and risk of lung cancer overall, by smoking status (never, former, and current smokers), and histological sub-type.

    Design Nested case-control study.

    Setting 20 population based cohort studies in Asia, Europe, Australia, and the United States.

    Participants 5299 patients with incident lung cancer, with individually incidence density matched controls.

    Exposure Circulating hsCRP concentrations in prediagnostic serum or plasma samples.

    Main outcome measure Incident lung cancer diagnosis.

    Results A positive association between circulating hsCRP concentration and the risk of lung cancer for current (odds ratio associated with a doubling in hsCRP concentration 1.09, 95% confidence interval 1.05 to 1.13) and former smokers (1.09, 1.04 to 1.14) was observed, but not for never smokers (P<0.01 for interaction). This association was strong and consistent across all histological subtypes, except for adenocarcinoma, which was not strongly associated with hsCRP concentration regardless of smoking status (odds ratio for adenocarcinoma overall 0.97, 95% confidence interval 0.94 to 1.01). The association between circulating hsCRP concentration and the risk of lung cancer was strongest in the first two years of follow-up for former and current smokers. Including hsCRP concentration in a risk model, in addition to smoking based variables, did not improve risk discrimination overall, but slightly improved discrimination for cancers diagnosed in the first two years of follow-up.

    Conclusions Former and current smokers with higher circulating hsCRP concentrations had a higher risk of lung cancer overall. Circulating hsCRP concentration was not associated with the risk of lung adenocarcinoma. Circulating hsCRP concentration could be a prediagnostic marker of lung cancer rather than a causal risk factor.

  • 11.
    Nordström, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Rehabiliteringsmedicin. Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Idrottsmedicin.
    Edin, Benoni B.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Fysiologi.
    Lindström, Sara
    Nordström, Peter
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Cognitive function and other risk factors for mild traumatic brain injury in young men: nationwide cohort study2013Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 346, s. f723-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective To investigate cognitive function and other risk factors for mild traumatic brain injury in young men.

    Design Nationwide prospective cohort study.

    Setting Sweden.

    Participants 305 885 men conscripted for military service from 1989 to 1994.

    Main outcome measure mild traumatic brain injuries in relation to cognitive function and other potential risk factors assessed at conscription and follow-up.

    Results Men with one mild traumatic brain injury within two years before (n=1988) or after cognitive testing (n=2214) had about 5.5% lower overall cognitive function scores than did men with no mild traumatic brain injury during follow up (P<0.001 for both). Moreover, men with at least two mild traumatic brain injuries after cognitive testing (n=795) had 15% lower overall cognitive function scores compared with those with no such injury (P<0.001). Independent strong risk factors (P<1x10(-10)) for at least one mild traumatic brain injury after cognitive testing (n=12 494 events) included low overall cognitive function, a previous mild traumatic brain injury, hospital admission for intoxications, and low education and socioeconomic status. In a sub-cohort of twin pairs in which one twin had a mild traumatic brain injury before cognitive testing (n=63), both twins had lower logical performance and technical performance compared with men in the total cohort with no mild traumatic brain injury (P<0.05 for all).

    Conclusion Low cognitive function, intoxications, and factors related to low socioeconomic status were strong independent risk factors for mild traumatic brain injuries in men. The low cognitive function in twin pairs discordant for mild traumatic brain injury suggests a genetic component to the low cognitive function associated with such injuries. The study included only men, so inferences to women should be made with caution.

  • 12. Ricci, Cristian
    et al.
    Wood, Angela
    Muller, David
    Gunter, Marc J.
    Agudo, Antonio
    Boeing, Heiner
    van der Schouw, Yvonne T.
    Warnakula, Samantha
    Saieva, Calogero
    Spijkerman, Annemieke
    Sluijs, Ivonne
    Tjonneland, Anne
    Kyro, Cecilie
    Weiderpass, Elisabete
    Kuehn, Tilman
    Kaaks, Rudolf
    Sanchez, Maria-Jose
    Panico, Salvatore
    Agnoli, Claudia
    Palli, Domenico
    Tumino, Rosario
    Engstrom, Gunnar
    Melander, Olle
    Bonnet, Fabrice
    Boer, Jolanda M. A.
    Key, Timothy J.
    Travis, Ruth C.
    Overvad, Kim
    Verschuren, W. M. Monique
    Quiros, J. Ramon
    Trichopoulou, Antonia
    Papatesta, Eleni-Maria
    Peppa, Eleni
    Iribas, Conchi Moreno
    Gavrila, Diana
    Forslund, Ann-Sofie
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Jansson, Jan-Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Matullo, Giuseppe
    Arriola, Larraitz
    Freisling, Heinz
    Lassale, Camille
    Tzoulaki, Ioanna
    Sharp, Stephen J.
    Forouhi, Nita G.
    Langenberg, Claudia
    Saracci, Rodolfo
    Sweeting, Michael
    Brennan, Paul
    Butterworth, Adam S.
    Riboli, Elio
    Wareham, Nick J.
    Danesh, John
    Ferrari, Pietro
    Alcohol intake in relation to non-fatal and fatal coronary heart disease and stroke: EPIC-CVD case-cohort study2018Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 361, artikkel-id k934Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE To investigate the association between alcohol consumption (at baseline and over lifetime) and non-fatal and fatal coronary heart disease (CHD) and stroke. DESIGN Multicentre case-cohort study. SETTING A study of cardiovascular disease (CVD) determinants within the European Prospective Investigation into Cancer and nutrition cohort (EPIC-CVD) from eight European countries. PARTICIPANTS 32 549 participants without baseline CVD, comprised of incident CVD cases and a subcohort for comparison. MAIN OUTCOME MEASURES Non-fatal and fatal CHD and stroke (including ischaemic and haemorrhagic stroke). RESULTS There were 9307 non-fatal CHD events, 1699 fatal CHD, 5855 non-fatal stroke, and 733 fatal stroke. Baseline alcohol intake was inversely associated with non-fatal CHD, with a hazard ratio of 0.94 (95% confidence interval 0.92 to 0.96) per 12 g/day higher intake. There was a J shaped association between baseline alcohol intake and risk of fatal CHD. The hazard ratios were 0.83 (0.70 to 0.98), 0.65 (0.53 to 0.81), and 0.82 (0.65 to 1.03) for categories 5.0-14.9 g/day, 15.0-29.9 g/day, and 30.0-59.9 g/day of total alcohol intake, respectively, compared with 0.1-4.9 g/ day. In contrast, hazard ratios for non-fatal and fatal stroke risk were 1.04 (1.02 to 1.07), and 1.05 (0.98 to 1.13) per 12 g/day increase in baseline alcohol intake, respectively, including broadly similar findings for ischaemic and haemorrhagic stroke. Associations with cardiovascular outcomes were broadly similar with average lifetime alcohol consumption as for baseline alcohol intake, and across the eight countries studied. There was no strong evidence for interactions of alcohol consumption with smoking status on the risk of CVD events. CONCLUSIONS Alcohol intake was inversely associated with non-fatal CHD risk but positively associated with the risk of different stroke subtypes. This highlights the opposing associations of alcohol intake with different CVD types and strengthens the evidence for policies to reduce alcohol consumption.

  • 13.
    Robinson, David
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Garmo, Hans
    Bill-Axelson, Anna
    Mucci, Lorelei
    Holmberg, Lars
    Stattin, Pär
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Use of 5 alpha-reductase inhibitors for lower urinary tract symptoms and risk of prostate cancer in Swedish men: nationwide, population based case-control study2013Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 346, s. f3406-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective To assess the association between 5 alpha-reductase inhibitor (5-ARI) use in men with lower urinary tract symptoms and prostate cancer risk. Design Nationwide, population based case-control study for men diagnosed with prostate cancer in 2007-09 within the Prostate Cancer data Base Sweden 2.0. Setting The National Prostate Cancer Register, National Patient Register, census, and Prescribed Drug Register in Sweden, from which we obtained data on 5-ARI use before date of prostate cancer diagnosis. Participants 26 735 cases and 133 671 matched controls; five controls per case were randomly selected from matched men in the background population. 7815 men (1499 cases and 6316 controls) had been exposed to 5-ARI. 412 men had been exposed to 5-ARI before the diagnosis of a cancer with Gleason score 8-10. Main outcome measures Risk of prostate cancer calculated as odds ratios and 95% confidence intervals by conditional logistic regression analyses. Results Risk of prostate cancer overall decreased with an increasing duration of exposure; men on 5-ARI treatment for more than three years had an odds ratio of 0.72 (95% confidence interval 0.59 to 0.89; P<0.001 for trend). The same pattern was seen for cancers with Gleason scores 2-6 and score 7 (both P<0.001 for trend). By contrast, the risk of tumours with Gleason scores 8-10 did not decrease with increasing exposure time to 5-ARI (for 0-1 year of exposure, odds ratio 0.96 (95% confidence interval 0.83 to 1.11); for 1-2 years, 1.07 (0.88 to 1.31); for 2-3 years, 0.96 (0.72 to 1.27); for >3 years, 1.23 (0.90 to 1.68); P=0.46 for trend). Conclusions Men treated with 5-ARI for lower urinary tract symptoms had a decreased risk of cancer with Gleason scores 2-7, and showed no evidence of an increased risk of cancer with Gleason scores 8-10 after up to four years' treatment.

  • 14. Trajanoska, Katerina
    et al.
    Morris, John A.
    Oei, Ling
    Zheng, Hou-Feng
    Evans, David M.
    Kiel, Douglas P.
    Ohlsson, Claes
    Richards, J. Brent
    Rivadeneira, Fernando
    Assessment of the genetic and clinical determinants of fracture risk: genome wide association and mendelian randomisation study2018Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 362, artikkel-id k3225Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVES: To identify the genetic determinants of fracture risk and assess the role of 15 clinical risk factors on osteoporotic fracture risk.

    DESIGN: Meta-analysis of genome wide association studies (GWAS) and a two-sample mendelian randomisation approach.

    SETTING: 25 cohorts from Europe, United States, east Asia, and Australia with genome wide genotyping and fracture data.

    PARTICIPANTS: A discovery set of 37 857 fracture cases and 227 116 controls; with replication in up to 147 200 fracture cases and 150 085 controls. Fracture cases were defined as individuals (>18 years old) who had fractures at any skeletal site confirmed by medical, radiological, or questionnaire reports. Instrumental variable analyses were performed to estimate effects of 15 selected clinical risk factors for fracture in a two-sample mendelian randomisation framework, using the largest previously published GWAS meta-analysis of each risk factor.

    RESULTS: Of 15 fracture associated loci identified, all were also associated with bone mineral density and mapped to genes clustering in pathways known to be critical to bone biology (eg, SOST, WNT16, and ESR1) or novel pathways (FAM210A, GRB10, and ETS2). Mendelian randomisation analyses showed a clear effect of bone mineral density on fracture risk. One standard deviation decrease in genetically determined bone mineral density of the femoral neck was associated with a 55% increase in fracture risk (odds ratio 1.55 (95% confidence interval 1.48 to 1.63; P=1.5×10-68). Hand grip strength was inversely associated with fracture risk, but this result was not significant after multiple testing correction. The remaining clinical risk factors (including vitamin D levels) showed no evidence for an effect on fracture.

    CONCLUSIONS: This large scale GWAS meta-analysis for fracture identified 15 genetic determinants of fracture, all of which also influenced bone mineral density. Among the clinical risk factors for fracture assessed, only bone mineral density showed a major causal effect on fracture. Genetic predisposition to lower levels of vitamin D and estimated calcium intake from dairy sources were not associated with fracture risk.

  • 15. Virtanen, Marianna
    et al.
    Nyberg, Solja T
    Batty, G David
    Jokela, Markus
    Heikkilä, Katriina
    Fransson, Eleonor I
    Alfredsson, Lars
    Bjorner, Jakob B
    Borritz, Marianne
    Burr, Hermann
    Casini, Annalisa
    Clays, Els
    De Bacquer, Dirk
    Dragano, Nico
    Elovainio, Marko
    Erbel, Raimund
    Ferrie, Jane E
    Hamer, Mark
    Jöckel, Karl-Heinz
    Kittel, France
    Knutsson, Anders
    Koskenvuo, Markku
    Koskinen, Aki
    Lunau, Thorsten
    Madsen, Ida EH
    Nielsen, Martin L
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Oksanen, Tuula
    Pahkin, Krista
    Pejtersen, Jan H
    Pentti, Jaana
    Rugulies, Reiner
    Salo, Paula
    Shipley, Martin J
    Siegrist, Johannes
    Steptoe, Andrew
    Suominen, Sakari B
    Theorell, Töres
    Toppinen-Tanner, Salla
    Väänänen, Ari
    Vahtera, Jussi
    Westerholm, Peter JM
    Westerlund, Hugo
    Slopen, Natalie
    Kawachi, Ichiro
    Singh-Manoux, Archana
    Kivimäki, Mika
    Perceived job insecurity as a risk factor for incident coronary heart disease: systematic review and meta-analysis2013Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 347, s. f4746-Artikkel i tidsskrift (Fagfellevurdert)
  • 16. Wensley, Frances
    et al.
    Gao, Pei
    Burgess, Stephen
    Kaptoge, Stephen
    Di Angelantonio, Emanuele
    Shah, Tina
    Engert, James C.
    Clarke, Robert
    Davey-Smith, George
    Nordestgaard, Borge G.
    Saleheen, Danish
    Samani, Nilesh J.
    Sandhu, Manjinder
    Anand, Sonia
    Pepys, Mark B.
    Smeeth, Liam
    Whittaker, John
    Casas, Juan Pablo
    Thompson, Simon G.
    Hingorani, Aroon D.
    Danesh, John
    Eiriksdottir, G.
    Harris, T. B.
    Launer, L. J.
    Gudnason, V.
    Folsom, A. R.
    Andrews, G.
    Ballantyne, C. M.
    Samani, N. J.
    Hall, A. S.
    Braund, P. S.
    Balmforth, A. J.
    Whincup, P. H.
    Morris, R.
    Lawlor, D. A.
    Lowe, G. D. O.
    Timpson, N.
    Ebrahim, S.
    Ben-Shlomo, Y.
    Davey-Smith, G.
    Nordestgaard, B. G.
    Tybjaerg-Hansen, A.
    Zacho, J.
    Brown, M.
    Sandhu, M.
    Ricketts, S. L.
    Ashford, S.
    Lange, L.
    Reiner, A.
    Cushman, M.
    Tracy, R.
    Wu, C.
    Ge, J.
    Zou, Y.
    Sun, A.
    Hung, J.
    McQuillan, B.
    Thompson, P.
    Beilby, J.
    Warrington, N.
    Palmer, L. J.
    Wanner, C.
    Drechsler, C.
    Hoffmann, M. M.
    Fowkes, F. G. R.
    Tzoulaki, I.
    Kumari, M.
    Miller, M.
    Marmot, M.
    Onland-Moret, C.
    van der Schouw, Y. T.
    Boer, J. M.
    Wijmenga, C.
    Khaw, K-T
    Vasan, R. S.
    Schnabel, R. B.
    Yamamoto, J. F.
    Benjamin, E. J.
    Schunkert, H.
    Erdmann, J.
    Koenig, I. R.
    Hengstenberg, C.
    Chiodini, B.
    Franzosi, M. G.
    Pietri, S.
    Gori, F.
    Rudock, M.
    Liu, Y.
    Lohman, K.
    Humphries, S. E.
    Hamsten, A.
    Norman, P. E.
    Hankey, G. J.
    Jamrozik, K.
    Rimm, E. B.
    Pai, J. K.
    Psaty, B. M.
    Heckbert, S. R.
    Bis, J. C.
    Yusuf, S.
    Anand, S.
    Engert, J. C.
    Xie, C.
    Collins, R.
    Clarke, R.
    Bennett, D.
    Kooner, J.
    Chambers, J.
    Elliott, P.
    Maerz, W.
    Kleber, M. E.
    Boehm, B. O.
    Winkelmann, B. R.
    Melander, O.
    Berglund, G.
    Koenig, W.
    Thorand, B.
    Baumert, J.
    Peters, A.
    Manson, J.
    Cooper, J. A.
    Talmud, P. J.
    Ladenvall, P.
    Johansson, L.
    Jansson, Jan-Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Reilly, M. P.
    Qu, L.
    Li, M.
    Rader, D. J.
    Watkins, H.
    Hopewell, J.
    Saleheen, D.
    Danesh, J.
    Frossard, P.
    Sattar, N.
    Robertson, M.
    Shepherd, J.
    Schaefer, E.
    Hofman, A.
    Witteman, J. C. M.
    Kardys, I.
    Dehghan, A.
    de Faire, U.
    Bennet, A.
    Gigante, B.
    Leander, K.
    Peters, B.
    Maitland-van der Zee, A. H.
    de Boer, A.
    Klungel, O.
    Greenland, P.
    Dai, J.
    Liu, S.
    Brunner, E.
    Kivimaki, M.
    O'Reilly, D.
    Ford, I.
    Packard, C. J.
    Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data2011Inngår i: BMJ. British Medical Journal, E-ISSN 1756-1833, Vol. 342, s. d548-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective To use genetic variants as unconfounded proxies of C reactive protein concentration to study its causal role in coronary heart disease. Design Mendelian randomisation meta-analysis of individual participant data from 47 epidemiological studies in 15 countries. Participants 194 418 participants, including 46 557 patients with prevalent or incident coronary heart disease. Information was available on four CRP gene tagging single nucleotide polymorphisms (rs3093077, rs1205, rs1130864, rs1800947), concentration of C reactive protein, and levels of other risk factors. Main outcome measures Risk ratios for coronary heart disease associated with genetically raised C reactive protein versus risk ratios with equivalent differences in C reactive protein concentration itself, adjusted for conventional risk factors and variability in risk factor levels within individuals. Results CRP variants were each associated with up to 30% per allele difference in concentration of C reactive protein (P<10(-34)) and were unrelated to other risk factors. Risk ratios for coronary heart disease per additional copy of an allele associated with raised C reactive protein were 0.93 (95% confidence interval 0.87 to 1.00) for rs3093077; 1.00 (0.98 to 1.02) for rs1205; 0.98 (0.96 to 1.00) for rs1130864; and 0.99 (0.94 to 1.03) for rs1800947. In a combined analysis, the risk ratio for coronary heart disease was 1.00 (0.90 to 1.13) per 1 SD higher genetically raised natural log (ln) concentration of C reactive protein. The genetic findings were discordant with the risk ratio observed for coronary heart disease of 1.33 (1.23 to 1.43) per 1 SD higher circulating ln concentration of C reactive protein in prospective studies (P=0.001 for difference). Conclusion Human genetic data indicate that C reactive protein concentration itself is unlikely to be even a modest causal factor in coronary heart disease.

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