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  • 51.
    Carlsson, Axel C
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Helmersson-Karlqvist, Johanna
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Ingelsson, Erik
    Larsson, Tobias E
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Urinary kidney injury molecule 1 and incidence of heart failure in elderly men2013Inngår i: European Journal of Heart Failure, ISSN 1388-9842, E-ISSN 1879-0844, Vol. 15, nr 4, s. 441-446Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    AIMS:

    There is growing recognition of the clinical importance of cardiorenal syndrome-the bidirectional interplay between kidney and cardiac dysfunction. Yet, the role of kidney tubular damage in the development of heart failure is less studied. The objective of this study was to investigate whether urinary kidney injury molecule (KIM)-1, a specific marker of tubular damage, predisposes to an increased heart failure risk.

    METHODS AND RESULTS:

    This was a community-based cohort study [Uppsala Longitudinal study of Adult Men (ULSAM)] of 565, 77-year-old men free from heart failure at baseline. Heart failure hospitalizations were used as outcome. During follow-up (median 8.0 years), 73 participants were hospitalized for heart failure. In models adjusted for cardiovascular risk factors (age, systolic blood pressure, diabetes, smoking, body mass index, LDL/HDL ratio, antihypertensive treatment, lipid-lowering treatment, aspirin treatment, LV hypertrophy, and prevalent cardiovascular disease) and markers of kidney dysfunction and damage [cystatin C-based glomerular filtration rate (GFR) and urinary albumin/creatinine ratio], a higher urinary KIM-1/creatinine ratio was associated with higher risk for heart failure (hazard ratio upper vs. lower tertile, 1.81; 95% confidence interval 1.01-3.29; P < 0.05). Participants with a combination of low GFR (<60 mL/min/1.72 m(2)) and high KIM-1/creatinine (>128 ng/mmol) had a 3-fold increase in heart failure risk compared with participants with normal GFR and KIM-1 (P < 0.001).

    CONCLUSION:

    Our findings suggest that kidney tubular damage predisposes to an increased risk for heart failure in the community. Further studies are needed to clarify the causal role of KIM-1 in the development of heart failure, and to evaluate the clinical utility of urinary KIM-1 measurements.

  • 52.
    Carlsson, Axel C
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Ruge, Toralph
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Association between circulating endostatin, hypertension duration, and hypertensive target-organ damage2013Inngår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 62, nr 6, s. 1146-1151Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Our aim is to study associations between circulating endostatin, hypertension duration, and hypertensive target-organ damage. Long-term hypertension induces cardiovascular and renal remodeling. Circulating endostatin, a biologically active derivate of collagen XVIII, has been suggested to be a relevant marker for extracellular matrix turnover and remodeling in various diseases. However, the role of endostatin in hypertension and hypertensive target-organ damage is unclear. Serum endostatin was measured in 2 independent community-based cohorts: the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS; women 51%; n=812; mean age, 75 years) and the Uppsala Longitudinal Study of Adult Men (ULSAM; n=785; mean age, 77.6 years). Retrospective data on blood pressure measurements and antihypertensive medication (PIVUS >5 years, ULSAM >27 years), and cross-sectional data on echocardiographic left ventricular mass, endothelial function (endothelium-dependent vasodilation assessed by the invasive forearm model), and urinary albumin/creatinine ratio were available. In PIVUS, participants with ≥5 years of history of hypertension portrayed 0.42 SD (95% confidence interval, 0.23-0.61; P<0.001) higher serum endostatin, compared with that of normotensives. This association was replicated in ULSAM, in which participants with 27 years hypertension duration had the highest endostatin (0.57 SD higher; 95% confidence interval, 0.35-0.80; P<0.001). In addition, higher endostatin was associated with higher left ventricular mass, worsened endothelial function, and higher urinary albumin/creatinine ratio (P<0.03 for all) in participants with prevalent hypertension. Circulating endostatin is associated with the duration of hypertension, and vascular, myocardial, and renal indices of hypertensive target-organ damage. Further studies are warranted to assess the prognostic role of endostatin in individuals with hypertension.

  • 53.
    Carlsson, Axel C.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Karolinska Inst, Div Family Med, Dept Neurobiol, Care Sci & Soc, Karlskrona, Sweden..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Carrero, Juan Jesus
    Karolinska Inst, Div Renal Med, Dept Clin Sci, Intervent & Technol, Karlskrona, Sweden..
    Gustafsson, Stefan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Stenemo, Markus
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Dalarna Univ, Sch Hlth & Social Sci, Dalarna, Sweden..
    Use of a proximity extension assay proteomics chip to discover new biomarkers associated with albuminuria2017Inngår i: European Journal of Preventive Cardiology, ISSN 2047-4873, E-ISSN 2047-4881, nr 4, s. 340-348Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: The underlying mechanisms for the development of albuminuria and the increased cardiovascular risk in patients with elevated albuminuria levels are incompletely understood. We therefore investigated the associations between 80 cardiovascular proteins and the urinary albumin to creatinine ratio (ACR).

    METHODS: We used a discovery/replication approach in two independent community-based cohorts of elderly patients: the Uppsala Longitudinal Study of Adult Men (n = 662; mean age 78 years) and the Prospective Investigation of the Vasculature in Uppsala Seniors (n = 757; mean age 75 years; 51% women). A proteomic chip with a panel of 80 plasma proteins associated with different aspects of cardiovascular disease was analysed. In the discovery cohort, we used a false discovery rate of 5% to take into account the multiple statistical testing. Nominal p values were used in the replication.

    RESULTS: Higher levels of T-cell immunoglobulin mucin-1, placenta growth factor, growth/differentiation factor-15, urokinase plasminogen activator surface receptor and kallikrein-11 were robustly associated with a higher ACR in both cohorts in multivariable linear regression models adjusted for sex, established cardiovascular risk factors, antihypertensive treatment, prevalent cardiovascular disease and glomerular filtration rate (p < 0.02 for all). All associations were also significant in separate analyses of patients without diabetes.

    CONCLUSIONS: We discovered and replicated associations between ACR and five cardiovascular proteins involved in tubular injury, atherosclerosis, endothelial function, heart failure, inflammation, glomerulosclerosis and podocyte injury. Our findings put forward multiplex proteomics as a promising approach to explore novel aspects of the complex detrimental interplay between kidney function and the cardiovascular system.

  • 54.
    Carlsson, Axel C
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Physical activity, obesity and risk of cardiovascular disease in middle-aged men during a median of 30 years of follow-up2016Inngår i: European Journal of Preventive Cardiology, ISSN 2047-4873, E-ISSN 2047-4881, Vol. 23, nr 4, s. 359-365Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND:

    We aimed to investigate associations between combinations of body mass index (BMI)-categories, levels of physical activity and long-term risk of cardiovascular disease.

    METHOD AND RESULTS:

    At age 50 years, cardiovascular risk factors were assessed in 2196 participating men of the ULSAM-study. This investigation was repeated at age 60, 70, 77 and 82 years. Being physically active (PA) was defined as three hours of recreational or hard physical training per week. The men were categorized according to BMI/PA-status, as PA/normal weight (n = 593 at baseline), non-PA/normal weight (BMI < 25 kg/m(2), n = 580), PA/overweight (n = 418), non-PA/overweight (BMI 25-30 kg/m(2), n = 462), PA/obese (n = 62), non-PA/obese (BMI >30 kg/m(2), n = 81). We used updated data on BMI and physical activity obtained at all examinations. During follow-up (median 30 years) 850 individuals suffered a cardiovascular disease (myocardial infarction, stroke or heart failure). Using updated data on BMI/PA categories, an increased risk for cardiovascular disease was seen with increasing BMI, but a high physical activity was associated with a lower risk of cardiovascular disease within each BMI category: non-PA/normal weight (hazard ratio (HR) 1.31, 95% confidence interval (CI) 1.04-1.66), PA/overweight (HR 1.52, 95% CI 1.20-1.94), non-PA/overweight (HR 1.65, 95% CI 1.31-2.07) PA/obese (HR 2.05, 95% CI 1.44-2.92) and non-PA/obese (HR 2.39, 95% CI 1.74-3.29), using PA/normal weight men as referent.

    CONCLUSIONS:

    Although physical activity was beneficial at all levels of BMI regarding the risk of future cardiovascular disease, there was still a substantial increased risk associated with being overweight or obese during 30 years of follow-up.

  • 55.
    Cars, T.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Neovius, M.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    TWENTY-YEAR TRENDS IN CARDIOVASCULAR RISK FACTORS AMONG SWEDISH MEN: IMPACT OF OVERWEIGHT AND OBESITY2010Inngår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, s. E482-E483Artikkel i tidsskrift (Annet vitenskapelig)
  • 56.
    Cars, Thomas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Neovius, M.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    LONGITUDINAL ANTIHYPERTENSIVE DRUG USE TRENDS AND TREATMENT DURATIONS BETWEEN 1970 AND 20052010Inngår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, s. E325-E325Artikkel i tidsskrift (Annet vitenskapelig)
  • 57.
    Cars, Thomas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Lindhagen, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Malmstrom, Rickard E.
    Karolinska Inst, Karolinska Univ Hosp, Dept Med, Div Clin Pharmacol, Stockholm, Sweden.
    Neovius, Martin
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden.
    Schwieler, Jonas
    Karolinska Inst, Dept Cardiol, Stockholm, Sweden.
    Wettermark, Bjorn
    Karolinska Inst, Dept Med, Ctr Pharmacoepidemiol, Stockholm, Sweden.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Dronedarone and Hepatic Toxicity?: A Model for Evaluation of Post-Marketing Safety of Drugs in Routine Care2017Inngår i: Pharmacoepidemiology and Drug Safety, ISSN 1053-8569, E-ISSN 1099-1557, Vol. 26, s. 381-382Artikkel i tidsskrift (Annet vitenskapelig)
  • 58.
    Cars, Thomas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Stockholm Cty Council, Publ Healthcare Serv Comm Adm, Stockholm, Sweden..
    Lindhagen, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Malmström, R. E.
    Karolinska Univ Hosp, Karolinska Inst, Dept Med Solna, Clin Pharmacol, Stockholm, Sweden..
    Neovius, M.
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden..
    Schwieler, J.
    Karolinska Inst, Dept Cardiol, Stockholm, Sweden..
    Wettermark, B.
    Stockholm Cty Council, Publ Healthcare Serv Comm Adm, Stockholm, Sweden.;Karolinska Inst, Dept Med, Ctr Pharmacoepidemiol, Stockholm, Sweden..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Effectiveness of Drugs in Routine Care: A Model for Sequential Monitoring of New Medicines Using Dronedarone as Example2018Inngår i: Clinical Pharmacology and Therapeutics, ISSN 0009-9236, E-ISSN 1532-6535, Vol. 103, nr 3, s. 493-501Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Although there is no doubt about the scientific value of randomized controlled clinical trials, they are usually conducted in selected populations different fromthose treated in clinical practice. Therefore, it is important to optimize real-time post-marketing evaluation of the effectiveness, safety, and cost of new drugs. Using electronic health records and administrative health databases froma well-defined region with universal access to healthcare, we have built a framework for real-time sequential monitoring of the effectiveness of newly marketed drugs in routine care. We chose the antiarrhythmic agent dronedarone as the study drug and flecainide as the comparator drug for illustration of the model. We demonstrate that this model produces consistent results with increasing precision over time as data accumulates in the clinical systems. We believe that use of this model at the introduction of new drugs can provide complementary evidence, especially in settings of adaptive licensing of new drugs.

  • 59.
    Cars, Thomas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk epidemiologi.
    Lindhagen, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk epidemiologi.
    A framework for monitoring of new drugs in Sweden2019Inngår i: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 124, nr 1, s. 46-50Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    In order to monitor the net public health benefit of new drugs, especially in the light of recent stepwise approval approaches, there is a need to optimize real-time post-marketing evaluation of new drugs using data collected in routine care. Sweden, with its unique possibilities for observational research, can provide these data. We herein propose a framework for continuous monitoring of the effectiveness, safety, and cost-effectiveness of new drugs, using prospectively determined protocols designed in collaboration between all relevant stakeholders. We believe that this framework can be a useful tool for healthcare authorities and reimbursement agencies in the introduction of new drugs.

  • 60.
    Cars, Thomas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Neovius, Martin
    Karolinska Inst, Dept Med, Stockholm, Sweden..
    Lindhagen, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Malmström, Rickard E.
    Karolinska Inst, Dept Med, Stockholm, Sweden..
    Schwieler, Jonas
    Karolinska Inst, Dept Cardiol, Stockholm, Sweden..
    Wettermark, Bjon
    Karolinska Inst, Dept Med, Stockholm, Sweden..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    An Automatized Model for Sequential Monitoring of Effectiveness of New Drugs Using Dronedarone as Example2016Inngår i: Pharmacoepidemiology and Drug Safety, ISSN 1053-8569, E-ISSN 1099-1557, Vol. 25, s. 504-504Artikkel i tidsskrift (Fagfellevurdert)
  • 61.
    Cars, Thomas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Stockholm Cty Council, Publ Healthcare Serv Comm Adm, Stockholm, Sweden..
    Wettermark, Bjorn
    Stockholm Cty Council, Publ Healthcare Serv Comm Adm, Stockholm, Sweden.;Karolinska Inst, Dept Med, Stockholm, Sweden..
    Lofberg, Robert
    Karolinska Inst, Dept Med, Stockholm, Sweden.;IBD Unit Sophiahemmet, Stockholm, Sweden..
    Eriksson, Irene
    Stockholm Cty Council, Publ Healthcare Serv Comm Adm, Stockholm, Sweden.;Karolinska Inst, Dept Med, Stockholm, Sweden..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Lordal, Mikael
    Karolinska Inst, Dept Med, Stockholm, Sweden.;Karolinska Univ Hosp, Ctr Digest Dis, Stockholm, Sweden..
    Healthcare Utilisation and Drug Treatment in a Large Cohort of Patients with Inflammatory Bowel Disease2016Inngår i: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 10, nr 5, s. 556-565Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Crohn's disease [CD] and ulcerative colitis [UC] are chronic diseases associated with a substantial utilisation of healthcare resources. We aimed to estimate the prevalence of inflammatory bowel disease [IBD], CD, and UC and to describe and compare healthcare utilisation and drug treatment in CD and UC patients. This was a cross-sectional study of all patients with a recorded IBD diagnosis in Stockholm County, Sweden. Data on outpatient visits, hospitalisations, surgeries, and drug treatment during 2013 were analysed. A total of 13 916 patients with IBD were identified, corresponding to an overall IBD prevalence of 0.65% [CD 0.27%, UC 0.35%, inflammatory bowel disease unclassified 0.04%]; 49% of all IBD patients were treated with IBD-related drugs. Only 3.6% of the patients received high-dose corticosteroids, whereas 32.4% were treated with aminosalicylates [CD 21.2%, UC 41.0%, p < 0.0001]. More CD patients were treated with biologicals compared with UC patients [CD 9.6%, UC 2.9%, p < 0.0001] and surgery was significantly more common among CD patients [CD 3.0%, UC 0.8%, p < 0.0001]. This study indicates that patients with CD are the group with the highest medical needs. Patients with CD utilised significantly more healthcare resources [including outpatient visits, hospitalisations, and surgeries] than UC patients. Twice as many CD patients received immunomodulators compared with UC patients and CD patients were treated with biologicals three times more often. These results highlight that CD remains a challenge and further efforts are needed to improve care in these patients.

  • 62. Chung, Sheng-Chia
    et al.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Gale, Chris P.
    James, Stefan K.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Deanfield, John
    Wallentin, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Timmis, Adam
    Jernberg, Tomas
    Hemingway, Harry
    Comparison of hospital variation in acute myocardial infarction care and outcome between Sweden and United Kingdom: population based cohort study using nationwide clinical registries2015Inngår i: BMJ-BRITISH MEDICAL JOURNAL, ISSN 1756-1833, Vol. 351, artikkel-id h3913Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE To assess the between hospital variation in use of guideline recommended treatments and clinical outcomes for acute myocardial infarction in Sweden and the United Kingdom. DESIGN Population based longitudinal cohort study using nationwide clinical registries. SETTING AND PARTICIPANTS Nationwide registry data comprising all hospitals providing acute myocardial infarction care in Sweden (SWEDEHEART/RIKS-HIA, n=87; 119 786 patients) and the UK (NICOR/MINAP, n=242; 391 077 patients), 2004-10. MAIN OUTCOME MEASURES Between hospital variation in 30 day mortality of patients admitted with acute myocardial infarction. RESULTS Case mix standardised 30 day mortality from acute myocardial infarction was lower in Swedish hospitals (8.4%) than in UK hospitals (9.7%), with less variation between hospitals (interquartile range 2.6% v 3.5%). In both countries, hospital level variation and 30 day mortality were inversely associated with provision of guideline recommended care. Compared with the highest quarter, hospitals in the lowest quarter for use of primary percutaneous coronary intervention had higher volume weighted 30 day mortality for ST elevation myocardial infarction (10.7% v 6.6% in Sweden; 12.7% v 5.8% in the UK). The adjusted odds ratio comparing the highest with the lowest quarters for hospitals' use of primary percutaneous coronary intervention was 0.70 (95% confidence interval 0.62 to 0.79) in Sweden and 0.68 (0.60 to 0.76) in the UK. Differences in risk between hospital quarters of treatment for non-ST elevation myocardial infarction and secondary prevention drugs for all discharged acute myocardial infarction patients were smaller than for reperfusion treatment in both countries. CONCLUSION Between hospital variation in 30 day mortality for acute myocardial infarction was greater in the UK than in Sweden. This was associated with, and may be partly accounted for by, the higher practice variation in acute myocardial infarction guideline recommended treatment in the UK hospitals. High quality healthcare across all hospitals, especially in the UK, with better use of guideline recommended treatment, may not only reduce unacceptable practice variation but also deliver improved clinical outcomes for patients with acute myocardial infarction.

  • 63.
    Chung, Sheng-Chia
    et al.
    UCL, Farr Inst Hlth Informat Res, London NW1 2DA, England.;UCL, Inst Hlth Informat, London NW1 2DA, England..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Gale, Chris P.
    Univ Leeds, Cardiovasc Hlth Sci, Leeds, W Yorkshire, England..
    Timmis, Adam
    Barts Hlth London, Cardiovasc Biomed Res Unit, Natl Inst Hlth Res, London, England..
    Jernberg, Tomas
    Karolinska Inst, Dept Med, Sect Cardiol, Stockholm, Sweden..
    Hemingway, Harry
    UCL, Farr Inst Hlth Informat Res, London NW1 2DA, England.;UCL, Inst Hlth Informat, London NW1 2DA, England..
    Hospital Variation in AMI Outcome in UK and Sweden: Authors’ reply to Gupta2015Inngår i: BMJ-BRITISH MEDICAL JOURNAL, ISSN 1756-1833, Vol. 351, artikkel-id h5140Artikkel i tidsskrift (Fagfellevurdert)
  • 64. Cornelis, M C
    et al.
    Gustafsson, Stefan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Ärnlöv, J
    Elmståhl, S
    Söderberg, S
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, Stanford, CA 94305 USA.
    Targeted proteomic analysis of habitual coffee consumption.2018Inngår i: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 283, nr 2, s. 200-211Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Coffee drinking has been implicated in mortality and a variety of diseases but potential mechanisms underlying these associations are unclear. Large-scale systems epidemiological approaches may offer novel insights to mechanisms underlying associations of coffee with health.

    OBJECTIVE: We performed an analysis of known and novel protein markers linked to cardiovascular disease and their association with habitual coffee intake in the Prospective Study of the Vasculature in Uppsala Seniors (PIVUS, n = 816) and followed up top proteins in the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 635) and EpiHealth (n = 2418).

    METHODS: In PIVUS and ULSAM, coffee intake was measured by 7-day dietary records whilst a computer-based food frequency questionnaire was used in EpiHealth. Levels of up to 80 proteins were assessed in plasma by a proximity extension assay.

    RESULTS: Four protein-coffee associations adjusted for age, sex, smoking and BMI, met statistical significance in PIVUS (FDR < 5%, P < 2.31 × 10(-3) ): leptin (LEP), chitinase-3-like protein 1 (CHI3L), tumour necrosis factor (TNF) receptor 6 and TNF-related apoptosis-inducing ligand. The inverse association between coffee intake and LEP replicated in ULSAM (β, -0.042 SD per cup of coffee, P = 0.028) and EpiHealth (β, -0.025 SD per time of coffee, P = 0.004). The negative coffee-CHI3L association replicated in EpiHealth (β, -0.07, P = 1.15 × 10(-7) ), but not in ULSAM (β, -0.034, P = 0.16).

    CONCLUSIONS: The current study supports an inverse association between coffee intake and plasma LEP and CHI3L1 levels. The coffee-CHI3L1 association is novel and warrants further investigation given links between CHI3L1 and health conditions that are also potentially influenced by coffee.

  • 65. Danaei, Goodarz
    et al.
    Fahimi, Saman
    Lu, Yuan
    Zhou, Bin
    Hajifathalian, Kaveh
    Di Cesare, Mariachiara
    Lo, Wei-Cheng
    Reis-Santos, Barbara
    Cowan, Melanie J.
    Shaw, Jonathan E.
    Bentham, James
    Lin, John K.
    Bixby, Honor
    Magliano, Dianna
    Bovet, Pascal
    Miranda, J. Jaime
    Khang, Young-Ho
    Stevens, Gretchen A.
    Riley, Leanne M.
    Ali, Mohammed K.
    Ezzati, Majid
    Abdeen, Ziad A.
    Kadir, Khalid Abdul
    Abu-Rmeileh, Niveen M.
    Acosta-Cazares, Benjamin
    Aekplakorn, Wichai
    Aguilar-Salinas, Carlos A.
    Ahmadvand, Alireza
    Al Nsour, Mohannad
    Alkerwi, Ala'a
    Amouyel, Philippe
    Andersen, Lars Bo
    Anderssen, Sigmund A.
    Andrade, Dolores S.
    Anjana, Ranjit Mohan
    Aounallah-Skhiri, Hajer
    Aris, Tahir
    Arlappa, Nimmathota
    Arveiler, Dominique
    Assah, Felix K.
    Avdicova, Maria
    Balakrishna, Nagalla
    Bandosz, Piotr
    Barbagallo, Carlo M.
    Barcelo, Alberto
    Batieha, Anwar M.
    Baur, Louise A.
    Ben Romdhane, Habiba
    Bernabe-Ortiz, Antonio
    Bhargava, Santosh K.
    Bi, Yufang
    Bjerregaard, Peter
    Bjorkelund, Cecilia
    Blake, Margaret
    Blokstra, Anneke
    Bo, Simona
    Boehm, Bernhard O.
    Boissonnet, Carlos P.
    Brajkovich, Imperia
    Breckenkamp, Juergen
    Brewster, Lizzy M.
    Brian, Garry R.
    Bruno, Graziella
    Bugge, Anna
    de Leon, Antonio Cabrera
    Can, Gunay
    Candido, Ana Paula C.
    Capuano, Vincenzo
    Carvalho, Maria J.
    Casanueva, Felipe F.
    Caserta, Carmelo A.
    Castetbon, Katia
    Chamukuttan, Snehalatha
    Chaturvedi, Nishi
    Chen, Chien-Jen
    Chen, Fangfang
    Chen, Shuohua
    Cheng, Ching-Yu
    Chetrit, Angela
    Chiou, Shu-Ti
    Cho, Yumi
    Chudek, Jerzy
    Cifkova, Renata
    Claessens, Frank
    Concin, Hans
    Cooper, Cyrus
    Cooper, Rachel
    Costanzo, Simona
    Cottel, Dominique
    Cowell, Chris
    Crujeiras, Ana B.
    D'Arrigo, Graziella
    Dallongeville, Jean
    Dankner, Rachel
    Dauchet, Luc
    de Gaetano, Giovanni
    De Henauw, Stefaan
    Deepa, Mohan
    Dehghan, Abbas
    Dhana, Klodian
    Di Castelnuovo, Augusto F.
    Djalalinia, Shirin
    Doua, Kouamelan
    Drygas, Wojciech
    Du, Yong
    Egbagbe, Eruke E.
    Eggertsen, Robert
    El Ati, Jalila
    Elosua, Roberto
    Erasmus, Rajiv T.
    Erem, Cihangir
    Ergor, Gul
    Eriksen, Louise
    la Penaa, Jorge Escobedo-De
    Fall, Caroline H.
    Farzadfar, Farshad
    Felix-Redondo, Francisco J.
    Ferguson, Trevor S.
    Fernandez-Berges, Daniel
    Ferrari, Marika
    Ferreccio, Catterina
    Finn, Joseph D.
    Foger, Bernhard
    Foo, Leng Huat
    Fouad, Heba M.
    Francis, Damian K.
    Franco, Maria do Carmo
    Franco, Oscar H.
    Frontera, Guillermo
    Furusawa, Takuro
    Gaciong, Zbigniew
    Galbarczyk, Andrzej
    Garnett, Sarah P.
    Gaspoz, Jean-Michel
    Gasull, Magda
    Gates, Louise
    Geleijnse, Johanna M.
    Ghasemain, Anoosheh
    Giampaoli, Simona
    Gianfagna, Francesco
    Giovannelli, Jonathan
    Gross, Marcela Gonzalez
    Rivas, Juan P. Gonzalez
    Gorbea, Mariano Bonet
    Gottrand, Frederic
    Grant, Janet F.
    Grodzicki, Tomasz
    Grontved, Anders
    Gruden, Grabriella
    Gu, Dongfeng
    Guan, Ong Peng
    Guerrero, Ramiro
    Guessous, Idris
    Guimaraes, Andre L.
    Gutierrez, Laura
    Hardy, Rebecca
    Kumar, Rachakulla Hari
    He, Jiang
    Heidemann, Christin
    Hihtaniemi, Ilpo Tapani
    Ho, Sai Yin
    Ho, Suzanne C.
    Hofman, Albert
    Russo, Andrea R. V.
    Hormiga, Claudia M.
    Horta, Bernardo L.
    Houti, Leila
    Hussieni, Abdullatif S.
    Huybrechts, Inge
    Hwalla, Nahla
    Iacoviello, Licia
    Iannone, Anna G.
    Ibrahim, Mohsen M.
    Ikeda, Nayu
    Ikram, M. Arfan
    Irazola, Vilma E.
    Islam, Muhammad
    Iwasaki, Masanori
    Jacobs, Jeremy M.
    Jafar, Tazeen
    Jasienska, Grazyna
    Jiang, Chao Qiang
    Jonas, Jost B.
    Joshi, Pradeep
    Kafatos, Anthony
    Kalter-Leibovici, Ofra
    Kasaeian, Amir
    Katz, Joanne
    Kaur, Prabhdeep
    Kavousi, Maryam
    Kelishadi, Roya
    Kengne, Andre P.
    Kersting, Mathilde
    Khader, Yousef Saleh
    Kiechl, Stefan
    Kim, Jeongseon
    Kiyohara, Yutaka
    Kolsteren, Patrick
    Korrovits, Paul
    Koskinen, Seppo
    Kratzer, Wolfgang
    Kromhout, Daan
    Kula, Krzysztof
    Kurjata, Pawel
    Kyobutungi, Catherine
    Lachat, Carl
    Laid, Youcef
    Lam, Tai Hing
    Landrove, Orlando
    Lanska, Vera
    Lappas, Georg
    Laxmaiah, Avula
    Leclercq, Catherine
    Lee, Jeannette
    Lee, Jeonghee
    Lehtimaki, Terho
    Lekhraj, Rampal
    Leon-Munoz, Luz M.
    Li, Yanping
    Lim, Wei-Yen
    Lima-Costa, M. Fernanda
    Lin, Hsien-Ho
    Lin, Xu
    Lissner, Lauren
    Lorbeer, Roberto
    Lozano, Jose Eugenio
    Lundqvist, Annamari
    Lytsy, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Socialmedicin.
    Ma, Guansheng
    Machado-Coelho, George L. L.
    Machi, Suka
    Maggi, Stefania
    Makdisse, Marcia
    Rao, Kodavanti Mallikharjuna
    Manios, Yannis
    Manzato, Enzo
    Margozzini, Paula
    Marques-Vidal, Pedro
    Martorell, Reynaldo
    Masoodi, Shariq R.
    Matsha, Tandi E.
    Mbanya, Jean Claude N.
    McFarlane, Shelly R.
    McGarvey, Stephen T.
    McLachlan, Stela
    McNulty, Breige A.
    Mediene-Benchekor, Sounnia
    Meirhaeghe, Aline
    Menezes, Ana Maria B.
    Merat, Shahin
    Meshram, Indrapal I.
    Mi, Jie
    Miquel, Juan Francisco
    Mohamed, Mostafa K.
    Mohammad, Kazem
    Mohan, Viswanathan
    Yusoff, Muhammad Fadhli Mohd
    Moller, Niels C.
    Molnar, Denes
    Mondo, Charles K.
    Moreno, Luis A.
    Morgan, Karen
    Moschonis, George
    Mossakowska, Malgorzata
    Mostafa, Aya
    Mota, Jorge
    Muiesan, Maria L.
    Muller-Nurasyid, Martina
    Mursu, Jaakko
    Nagel, Gabriele
    Namesna, Jana
    Nang, Ei Ei K.
    Nangia, Vinay B.
    Navarrete-Munoz, Eva Maria
    Ndiaye, Ndeye Coumba
    Nervi, Flavio
    Nguyen, Nguyen D.
    Nieto-Martinez, Ramfi S. E.
    Ning, Guang
    Ninomiya, Toshiharu
    Noale, Marianna
    Noto, Davide
    Ochoa-Aviles, Angelica M.
    Oh, Kyungwon
    Onat, Altan
    Osmond, Clive
    Otero, Johanna A.
    Palmieri, Luigi
    Panda-Jonas, Songhomitra
    Panza, Francesco
    Parsaeian, Mahboubeh
    Peixoto, Sergio Viana
    Pereira, Alexandre C.
    Peters, Annette
    Peykari, Niloofar
    Pilav, Aida
    Pitakaka, Freda
    Piwonska, Aleksandra
    Piwonski, Jerzy
    Plans-Rubio, Pedro
    Porta, Miquel
    Portegies, Marileen L. P.
    Poustchi, Hossein
    Pradeepa, Rajendra
    Price, Jacqueline F.
    Punab, Margus
    Qasrawi, Radwan F.
    Qorbani, Mostafa
    Raitakari, Olli
    Rao, Sudha Ramachandra
    Ramachandran, Ambady
    Ramos, Rafel
    Rampal, Sanjay
    Rathmann, Wolfgang
    Redon, Josep
    Reganit, Paul Ferdinand M.
    Rigo, Fernando
    Robinson, Sian M.
    Robitaille, Cynthia
    Rodriguez, Laura A.
    Rodriguez-Artalejo, Fernando
    Rodriguez-Perez, Maria del Cristo
    Rojas-Martinez, Rosalba
    Romaguera, Dora
    Rosengren, Annika
    Rubinstein, Adolfo
    Rui, Ornelas
    Ruiz-Betancourt, Blanca Sandra
    Rutkowski, Marcin
    Sabanayagam, Charumathi
    Sachdev, Harshpal S.
    Saidi, Olfa
    Sakarya, Sibel
    Salanave, Benoit
    Salonen, Jukka T.
    Salvetti, Massimo
    Sanchez-Abanto, Jose
    Nunes, Renata
    Santos, Rute
    Sardinha, Luis B.
    Scazufca, Marcia
    Schargrodsky, Herman
    Scheidt-Nave, Christa
    Shibuya, Kenji
    Shin, Youchan
    Shiri, Rahman
    Siantar, Rosalynn
    Sibai, Abla M.
    Simon, Mary
    Simons, Judith
    Simons, Leon A.
    Sjostrom, Michael
    Slowikowska-Hilczer, Jolanta
    Slusarczyk, Przemyslaw
    Smeeth, Liam
    Snijder, Marieke B.
    Solfrizzi, Vincenzo
    Sonestedt, Emily
    Soumare, Aicha
    Staessen, Jan A.
    Steene-Johannessen, Jostein
    Stehle, Peter
    Stein, Aryeh D.
    Stessman, Jochanan
    Stockl, Doris
    Stokwiszewski, Jakub
    Strufaldi, Maria Wany
    Sun, Chien-An
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Suriyawongpaisal, Paibul
    Sy, Rody G.
    Tai, E. Shyong
    Tarawneh, Mohammed
    Tarqui-Mamani, Carolina B.
    Thijs, Lutgarde
    Tolstrup, Janne S.
    Topbas, Murat
    Torrent, Maties
    Traissac, Pierre
    Trinh, Oanh T. H.
    Tulloch-Reid, Marshall K.
    Tuomainen, Tomi-Pekka
    Turley, Maria L.
    Tzourio, Christophe
    Ueda, Peter
    Ukoli, Flora M.
    Ulmer, Hanno
    Valdivia, Gonzalo
    Van Valkengoed, Irene G. M.
    Vanderschueren, Dirk
    Vanuzzo, Diego
    Vega, Tomas
    Velasquez-Melendez, Gustavo
    Veronesi, Giovanni
    Verschuren, Monique
    Vioque, Jesus
    Virtanen, Jyrki
    Visvikis-Siest, Sophie
    Viswanathan, Bharathi
    Vollenweider, Peter
    Voutilainen, Sari
    Wade, Alisha N.
    Wagner, Aline
    Walton, Janette
    Mohamud, Wan Nazaimoon Wan
    Wang, Ming-Dong
    Wang, Ya Xing
    Wannamethee, S. Goya
    Weerasekera, Deepa
    Whincup, Peter H.
    Widhalm, Kurt
    Wiecek, Andrzej
    Wilks, Rainford J.
    Willeit, Johann
    Wojtyniak, Bogdan
    Wong, Tien Yin
    Woo, Jean
    Woodward, Mark
    Wu, Aleksander Giwercman
    Wu, Frederick C.
    Wu, Shou Ling
    Xu, Haiquan
    Yang, Xiaoguang
    Ye, Xingwang
    Yoshihara, Akihiro
    Younger-Coleman, Novie O.
    Zambon, Sabina
    Zargar, Abdul Hamid
    Zdrojewski, Tomasz
    Zhao, Wenhua
    Zheng, Yingfeng
    Effects of diabetes definition on global surveillance of diabetes prevalence and diagnosis: a pooled analysis of 96 population-based studies with 331288 participants2015Inngår i: LANCET DIABETES & ENDOCRINOLOGY, ISSN 2213-8587, Vol. 3, nr 8, s. 624-637Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background Diabetes has been defined on the basis of different biomarkers, including fasting plasma glucose (FPG), 2-h plasma glucose in an oral glucose tolerance test (2hOGTT), and HbA(1c). We assessed the effect of different diagnostic definitions on both the population prevalence of diabetes and the classification of previously undiagnosed individuals as having diabetes versus not having diabetes in a pooled analysis of data from population-based health examination surveys in different regions. Methods We used data from 96 population-based health examination surveys that had measured at least two of the biomarkers used for defining diabetes. Diabetes was defined using HbA(1c) (HbA(1c) >= 6 . 5% or history of diabetes diagnosis or using insulin or oral hypoglycaemic drugs) compared with either FPG only or FPG-or-2hOGTT definitions (FPG >= 7 . 0 mmol/L or 2hOGTT >= 11 . 1 mmol/L or history of diabetes or using insulin or oral hypoglycaemic drugs). We calculated diabetes prevalence, taking into account complex survey design and survey sample weights. We compared the prevalences of diabetes using different definitions graphically and by regression analyses. We calculated sensitivity and specificity of diabetes diagnosis based on HbA1c compared with diagnosis based on glucose among previously undiagnosed individuals (ie, excluding those with history of diabetes or using insulin or oral hypoglycaemic drugs). We calculated sensitivity and specificity in each survey, and then pooled results using a random-effects model. We assessed the sources of heterogeneity of sensitivity by meta-regressions for study characteristics selected a priori. Findings Population prevalence of diabetes based on FPG- or-2hOGTT was correlated with prevalence based on FPG alone (r= 0 . 98), but was higher by 2-6 percentage points at different prevalence levels. Prevalence based on HbA(1c) was lower than prevalence based on FPG in 42 . 8% of age-sex-survey groups and higher in another 41 . 6%; in the other 15 . 6%, the two definitions provided similar prevalence estimates. The variation across studies in the relation between glucose-based and HbA(1c)-based prevalences was partly related to participants' age, followed by natural logarithm of per person gross domestic product, the year of survey, mean BMI, and whether the survey population was national, subnational, or from specific communities. Diabetes defined as HbA(1c) 6 . 5% or more had a pooled sensitivity of 52 . 8% (95% CI 51 . 3-54 . 3%) and a pooled specificity of 99 . 74% (99 . 71-99 . 78%) compared with FPG 7 . 0 mmol/L or more for diagnosing previously undiagnosed participants; sensitivity compared with diabetes defined based on FPG-or-2hOGTT was 30 . 5% (28 . 7-32 . 3%). None of the preselected study-level characteristics explained the heterogeneity in the sensitivity of HbA(1c) versus FPG. Interpretation Different biomarkers and definitions for diabetes can provide different estimates of population prevalence of diabetes, and differentially identify people without previous diagnosis as having diabetes. Using an HbA(1c)-based definition alone in health surveys will not identify a substantial proportion of previously undiagnosed people who would be considered as having diabetes using a glucose-based test.

  • 66. Di Angelantonio, Emanuele
    et al.
    Gao, Pei
    Khan, Hassan
    Butterworth, Adam S.
    Wormser, David
    Kaptoge, Stephen
    Seshasai, Sreenivasa Rao Kondapally
    Thompson, Alex
    Sarwar, Nadeem
    Willeit, Peter
    Ridker, Paul M.
    Barr, Elizabeth L. M.
    Khaw, Kay-Tee
    Psaty, Bruce M.
    Brenner, Hermann
    Balkau, Beverley
    Dekker, Jacqueline M.
    Lawlor, Debbie A.
    Daimon, Makoto
    Willeit, Johann
    Njolstad, Inger
    Nissinen, Aulikki
    Brunner, Eric J.
    Kuller, Lewis H.
    Price, Jackie F.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Knuiman, Matthew W.
    Feskens, Edith J. M.
    Verschuren, W. M. M.
    Wald, Nicholas
    Bakker, Stephan J. L.
    Whincup, Peter H.
    Ford, Ian
    Goldbourt, Uri
    Gomez-de-la-Camara, Agustin
    Gallacher, John
    Simons, Leon A.
    Rosengren, Annika
    Sutherland, Susan E.
    Bjorkelund, Cecilia
    Blazer, Dan G.
    Wassertheil-Smoller, Sylvia
    Onat, Altan
    Ibanez, Alejandro Marin
    Casiglia, Edoardo
    Jukema, J. Wouter
    Simpson, Lara M.
    Giampaoli, Simona
    Nordestgaard, Borge G.
    Selmer, Randi
    Wennberg, Patrik
    Kauhanen, Jussi
    Salonen, Jukka T.
    Dankner, Rachel
    Barrett-Connor, Elizabeth
    Kavousi, Maryam
    Gudnason, Vilmundur
    Evans, Denis
    Wallace, Robert B.
    Cushman, Mary
    D'Agostino, Ralph B., Sr.
    Umans, Jason G.
    Kiyohara, Yutaka
    Nakagawa, Hidaeki
    Sato, Shinichi
    Gillum, Richard F.
    Folsom, Aaron R.
    van der Schouw, Yvonne T.
    Moons, Karel G.
    Griffin, Simon J.
    Sattar, Naveed
    Wareham, Nicholas J.
    Selvin, Elizabeth
    Thompson, Simon G.
    Danesh, John
    Glycated Hemoglobin Measurement and Prediction of Cardiovascular Disease2014Inngår i: Journal of the American Medical Association (JAMA), ISSN 0098-7484, E-ISSN 1538-3598, Vol. 311, nr 12, s. 1225-1233Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    IMPORTANCE The value of measuring levels of glycated hemoglobin (HbA(1c)) for the prediction of first cardiovascular events is uncertain. OBJECTIVE To determine whether adding information on HbA(1c) values to conventional cardiovascular risk factors is associated with improvement in prediction of cardiovascular disease (CVD) risk. DESIGN, SETTING, AND PARTICIPANTS Analysis of individual-participant data available from 73 prospective studies involving 294 998 participants without a known history of diabetes mellitus or CVD at the baseline assessment. MAIN OUTCOMES AND MEASURES Measures of risk discrimination for CVD outcomes (eg, C-index) and reclassification (eg, net reclassification improvement) of participants across predicted 10-year risk categories of low (<5%), intermediate (5% to <7.5%), and high (>= 7.5%) risk. RESULTS During a median follow-up of 9.9 (interquartile range, 7.6-13.2) years, 20 840 incident fatal and nonfatal CVD outcomes (13 237 coronary heart disease and 7603 stroke outcomes) were recorded. In analyses adjusted for several conventional cardiovascular risk factors, there was an approximately J-shaped association between HbA(1c) values and CVD risk. The association between HbA(1c) values and CVD risk changed only slightly after adjustment for total cholesterol and triglyceride concentrations or estimated glomerular filtration rate, but this association attenuated somewhat after adjustment for concentrations of high-density lipoprotein cholesterol and C-reactive protein. The C-index for a CVD risk prediction model containing conventional cardiovascular risk factors alone was 0.7434 (95% CI, 0.7350 to 0.7517). The addition of information on HbA(1c) was associated with a C-index change of 0.0018 (0.0003 to 0.0033) and a net reclassification improvement of 0.42 (-0.63 to 1.48) for the categories of predicted 10-year CVD risk. The improvement provided by HbA(1c) assessment in prediction of CVD risk was equal to or better than estimated improvements for measurement of fasting, random, or postload plasma glucose levels. CONCLUSIONS AND RELEVANCE In a study of individuals without known CVD or diabetes, additional assessment of HbA(1c) values in the context of CVD risk assessment provided little incremental benefit for prediction of CVD risk.

  • 67. Di Angelantonio, Emanuele
    et al.
    Gao, Pei
    Pennells, Lisa
    Kaptoge, Stephen
    Caslake, Muriel
    Thompson, Alexander
    Butterworth, Adam S.
    Sarwar, Nadeem
    Wormser, David
    Saleheen, Danish
    Ballantyne, Christie M.
    Psaty, Bruce M.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Ridker, Paul M.
    Nagel, Dorothea
    Gillum, Richard F.
    Ford, Ian
    Ducimetiere, Pierre
    Kiechl, Stefan
    Dullaart, Robin P. F.
    Assmann, Gerd
    D'Agostino, Ralph B.
    Dagenais, Gilles R.
    Cooper, Jackie A.
    Kromhout, Daan
    Onat, Altan
    Tipping, Robert W.
    Gomez-de-la-Camara, Agustin
    Rosengren, Annika
    Sutherland, Susan E.
    Gallacher, John
    Fowkes, F. Gerry R.
    Casiglia, Edoardo
    Hofman, Albert
    Salomaa, Veikko
    Barrett-Connor, Elizabeth
    Clarke, Robert
    Brunner, Eric
    Jukema, J. Wouter
    Simons, Leon A.
    Sandhu, Manjinder
    Wareham, Nicholas J.
    Khaw, Kay-Tee
    Kauhanen, Jussi
    Salonen, Jukka T.
    Howard, William J.
    Nordestgaard, Borge G.
    Wood, Angela M.
    Thompson, Simon G.
    Boekholdt, S. Matthijs
    Sattar, Naveed
    Packard, Chris
    Gudnason, Vilmundur
    Danesh, John
    Lipid-Related Markers and Cardiovascular Disease Prediction2012Inngår i: Journal of the American Medical Association (JAMA), ISSN 0098-7484, E-ISSN 1538-3598, Vol. 307, nr 23, s. 2499-2506Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Context

    The value of assessing various emerging lipid-related markers for prediction of first cardiovascular events is debated.

    Objective 

    To determine whether adding information on apolipoprotein B and apolipoprotein A-I, lipoprotein(a), or lipoprotein-associated phospholipase A2 to total cholesterol and high-density lipoprotein cholesterol (HDL-C) improves cardiovascular disease (CVD) risk prediction.

    Design, Setting, and Participants 

    Individual records were available for 165 544 participants without baseline CVD in 37 prospective cohorts (calendar years of recruitment: 1968-2007) with up to 15 126 incident fatal or nonfatal CVD outcomes (10 132 CHD and 4994 stroke outcomes) during a median follow-up of 10.4 years (interquartile range, 7.6-14 years).

    Main Outcome Measures 

    Discrimination of CVD outcomes and reclassification of participants across predicted 10-year risk categories of low (<10%), intermediate (10%-<20%), and high (≥20%) risk.

    Results 

    The addition of information on various lipid-related markers to total cholesterol, HDL-C, and other conventional risk factors yielded improvement in the model's discrimination: C-index change, 0.0006 (95% CI, 0.0002-0.0009) for the combination of apolipoprotein B and A-I; 0.0016 (95% CI, 0.0009-0.0023) for lipoprotein(a); and 0.0018 (95% CI, 0.0010-0.0026) for lipoprotein-associated phospholipase A2 mass. Net reclassification improvements were less than 1% with the addition of each of these markers to risk scores containing conventional risk factors. We estimated that for 100 000 adults aged 40 years or older, 15 436 would be initially classified at intermediate risk using conventional risk factors alone. Additional testing with a combination of apolipoprotein B and A-I would reclassify 1.1%; lipoprotein(a), 4.1%; and lipoprotein-associated phospholipase A2 mass, 2.7% of people to a 20% or higher predicted CVD risk category and, therefore, in need of statin treatment under Adult Treatment Panel III guidelines.

    Conclusion 

    In a study of individuals without known CVD, the addition of information on the combination of apolipoprotein B and A-I, lipoprotein(a), or lipoprotein-associated phospholipase A2 mass to risk scores containing total cholesterol and HDL-C led to slight improvement in CVD prediction.

  • 68. Di Angelantonio, Emanuele
    et al.
    Kaptoge, Stephen
    Wormser, David
    Willeit, Peter
    Butterworth, Adam S.
    Bansal, Narinder
    O'Keeffe, Linda M.
    Gao, Pei
    Wood, Angela M.
    Burgess, Stephen
    Freitag, Daniel F.
    Pennells, Lisa
    Peters, Sanne A.
    Hart, Carole L.
    Haheim, Lise Lund
    Gillum, Richard F.
    Nordestgaard, Borge G.
    Psaty, Bruce M.
    Yeap, Bu B.
    Knuiman, Matthew W.
    Nietert, Paul J.
    Kauhanen, Jussi
    Salonen, Jukka T.
    Kuller, Lewis H.
    Simons, Leon A.
    van der Schouw, Yvonne T.
    Barrett-Connor, Elizabeth
    Selmer, Randi
    Crespo, Carlos J.
    Rodriguez, Beatriz
    Verschuren, W. M. Monique
    Salomaa, Veikko
    Svärdsudd, Kurt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    van der Harst, Pim
    Bjorkelund, Cecilia
    Wilhelmsen, Lars
    Wallace, Robert B.
    Brenner, Hermann
    Amouyel, Philippe
    Barr, Elizabeth L. M.
    Iso, Hiroyasu
    Onat, Altan
    Trevisan, Maurizio
    D'Agostino, Ralph B., Sr.
    Cooper, Cyrus
    Kavousi, Maryam
    Welin, Lennart
    Roussel, Ronan
    Hu, Frank B.
    Sato, Shinichi
    Davidson, Karina W.
    Howard, Barbara V.
    Leening, Maarten
    Rosengren, Annika
    Dorr, Marcus
    Deeg, Dorly J. H.
    Kiechl, Stefan
    Stehouwer, Coen D. A.
    Nissinen, Aulikki
    Giampaoli, Simona
    Donfrancesco, Chiara
    Kromhout, Daan
    Price, Jackie F.
    Peters, Annette
    Meade, Tom W.
    Casiglia, Edoardo
    Lawlor, Debbie A.
    Gallacher, John
    Nagel, Dorothea
    Franco, Oscar H.
    Assmann, Gerd
    Dagenais, Gilles R.
    Jukema, J. Wouter
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Woodward, Mark
    Brunner, Eric J.
    Khaw, Kay-Tee
    Wareham, Nicholas J.
    Whitsel, Eric A.
    Njolstad, Inger
    Hedblad, Bo
    Wassertheil-Smoller, Sylvia
    Engstrom, Gunnar
    Rosamond, Wayne D.
    Selvin, Elizabeth
    Sattar, Naveed
    Thompson, Simon G.
    Danesh, John
    Association of Cardiometabolic Multimorbidity With Mortality: The Emerging Risk Factors Collaboration2015Inngår i: Journal of the American Medical Association (JAMA), ISSN 0098-7484, E-ISSN 1538-3598, Vol. 314, nr 1, s. 52-60Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    IMPORTANCE The prevalence of cardiometabolic multimorbidity is increasing.

    OBJECTIVE To estimate reductions in life expectancy associated with cardiometabolic multimorbidity.

    DESIGN, SETTING, AND PARTICIPANTS Age-and sex-adjusted mortality rates and hazard ratios (HRs) were calculated using individual participant data from the Emerging Risk Factors Collaboration (689 300 participants; 91 cohorts; years of baseline surveys: 1960-2007; latest mortality follow-up: April 2013; 128 843 deaths). The HRs from the Emerging Risk Factors Collaboration were compared with those from the UK Biobank (499 808 participants; years of baseline surveys: 2006-2010; latest mortality follow-up: November 2013; 7995 deaths). Cumulative survival was estimated by applying calculated age-specific HRs for mortality to contemporary US age-specific death rates. EXPOSURES A history of 2 or more of the following: diabetes mellitus, stroke, myocardial infarction (MI).

    MAIN OUTCOMES AND MEASURES All-cause mortality and estimated reductions in life expectancy.

    RESULTS In participants in the Emerging Risk Factors Collaboration without a history of diabetes, stroke, or MI at baseline (reference group), the all-cause mortality rate adjusted to the age of 60 years was 6.8 per 1000 person-years. Mortality rates per 1000 person-years were 15.6 in participants with a history of diabetes, 16.1 in those with stroke, 16.8 in those with MI, 32.0 in those with both diabetes and MI, 32.5 in those with both diabetes and stroke, 32.8 in those with both stroke and MI, and 59.5 in those with diabetes, stroke, and MI. Compared with the reference group, the HRs for all-cause mortality were 1.9 (95% CI, 1.8-2.0) in participants with a history of diabetes, 2.1 (95% CI, 2.0-2.2) in those with stroke, 2.0 (95% CI, 1.9-2.2) in those with MI, 3.7 (95% CI, 3.3-4.1) in those with both diabetes and MI, 3.8 (95% CI, 3.5-4.2) in those with both diabetes and stroke, 3.5 (95% CI, 3.1-4.0) in those with both stroke and MI, and 6.9 (95% CI, 5.7-8.3) in those with diabetes, stroke, and MI. The HRs from the Emerging Risk Factors Collaboration were similar to those from the more recently recruited UK Biobank. The HRs were little changed after further adjustment for markers of established intermediate pathways (eg, levels of lipids and blood pressure) and lifestyle factors (eg, smoking, diet). At the age of 60 years, a history of any 2 of these conditions was associated with 12 years of reduced life expectancy and a history of all 3 of these conditions was associated with 15 years of reduced life expectancy.

    CONCLUSIONS AND RELEVANCE Mortality associated with a history of diabetes, stroke, or MI was similar for each condition. Because any combination of these conditions was associated with multiplicative mortality risk, life expectancy was substantially lower in people with multimorbidity.

  • 69.
    Di Cesare, Mariachiara
    et al.
    Univ London Imperial Coll Sci Technol & Med, London, England.;Middlesex Univ, London N17 8HR, England..
    Bentham, James
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Stevens, Gretchen A.
    WHO, CH-1211 Geneva, Switzerland..
    Zhou, Bin
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Danaei, Goodarz
    Harvard Univ, TH Chan Sch Publ Hlth, Boston, MA 02115 USA..
    Lu, Yuan
    Harvard Univ, TH Chan Sch Publ Hlth, Boston, MA 02115 USA..
    Bixby, Honor
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Cowan, Melanie J.
    WHO, CH-1211 Geneva, Switzerland..
    Riley, Leanne M.
    WHO, CH-1211 Geneva, Switzerland..
    Hajifathalian, Kaveh
    Harvard Univ, TH Chan Sch Publ Hlth, Boston, MA 02115 USA..
    Fortunato, Lea
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Taddei, Cristina
    Univ Florence, Florence, Italy..
    Bennett, James E.
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Ikeda, Nayu
    Natl Inst Hlth & Nutr, Tokyo 162, Japan..
    Khang, Young-Ho
    Seoul Natl Univ, Seoul, South Korea..
    Kyobutungi, Catherine
    African Populat & Hlth Res Ctr, Nairobi, Kenya..
    Laxmaiah, Avula
    Indian Council Med Res, New Delhi, India..
    Li, Yanping
    Harvard Univ, TH Chan Sch Publ Hlth, Boston, MA 02115 USA..
    Lin, Hsien-Ho
    Natl Taiwan Univ, Taipei 10764, Taiwan..
    Miranda, J. Jaime
    Univ Peruana Cayetano Heredia, Lima, Peru..
    Mostafa, Aya
    Ain Shams Univ, Cairo, Egypt..
    Turley, Maria L.
    Minist Hlth, Wellington, New Zealand..
    Paciorek, Christopher J.
    Univ Calif Berkeley, Berkeley, CA 94720 USA..
    Gunter, Marc
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Ezzati, Majid
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Abdeen, Ziad A.
    Al Quds Univ, Jerusalem, Israel..
    Hamid, Zargar Abdul
    Ctr Diabet & Endocrine Care, Bengaluru, India..
    Abu-Rmeileh, Niveen M.
    Birzeit Univ, Bir Zayt, Israel..
    Acosta-Cazares, Benjamin
    Inst Mexicano Seguro Social, Rio Grande, Mexico..
    Adams, Robert
    Univ Adelaide, Adelaide, SA 5005, Australia..
    Aekplakorn, Wichai
    Mahidol Univ, Bangkok 10700, Thailand..
    Aguilar-Salinas, Carlos A.
    Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Rio Grande, Mexico..
    Ahmadvand, Alireza
    Noncommunicable Dis Res Ctr, Tehran, Iran..
    Ahrens, Wolfgang
    Leibniz Inst Prevent Res & Epidemiol BIPS, Leibniz, Germany..
    Ali, Mohamed M.
    World Hlth Org Reg Off Eastern Mediterranean, Giza, Egypt..
    Alkerwi, Ala'a
    Luxembourg Inst Hlth, Luxembourg, Luxembourg..
    Alvarez-Pedrerol, Mar
    Ctr Res Environm Epidemiol, Madrid, Spain..
    Aly, Eman
    World Hlth Org Reg Off Eastern Mediterranean, Giza, Egypt..
    Amouyel, Philippe
    Lille Univ & Hosp, Lille, France..
    Amuzu, Antoinette
    London Sch Hyg & Trop Med, London, England..
    Andersen, Lars Bo
    Univ Southern Denmark, Lyngby, Denmark..
    Anderssen, Sigmund A.
    Norwegian Sch Sport Sci, Oslo, Norway..
    Andrade, Dolores S.
    Univ Cuenca, Cuenca, Ecuador..
    Anjana, Ranjit Mohan
    Madras Diabet Res Fdn, Madras, Tamil Nadu, India..
    Aounallah-Skhiri, Hajer
    Natl Inst Publ Hlth, Tunis, Tunisia..
    Ariansen, Inger
    Norwegian Inst Publ Hlth, Oslo, Norway..
    Aris, Tahir
    Minist Hlth, Kuala Lumpur, Malaysia..
    Arlappa, Nimmathota
    Indian Council Med Res, New Delhi, India..
    Arveiler, Dominique
    Strasbourg Univ & Hosp, Strasbourg, France..
    Assah, Felix K.
    Univ Yaounde I, Yaounde, Cameroon..
    Avdicova, Maria
    Reg Author Publ Hlth, Banska Bystrica, Slovakia..
    Azizi, Fereidoun
    Shahid Beheshti Univ Med Sci, Tehran, Iran..
    Babu, Bontha V.
    Indian Council Med Res, New Delhi, India..
    Balakrishna, Nagalla
    Indian Council Med Res, New Delhi, India..
    Bandosz, Piotr
    Med Univ Gdansk, Gdansk, Poland..
    Banegas, Jose R.
    Univ Autonoma Madrid, E-28049 Madrid, Spain..
    Barbagallo, Carlo M.
    Univ Palermo, I-90133 Palermo, Italy..
    Barcelo, Alberto
    Pan Amer Hlth Org, El Paso, TX USA..
    Barkat, Amina
    Univ Mohammed V Rabat, Rabat, Morocco..
    Barros, Mauro V.
    Univ Pernambuco, Petrolina, PE, Brazil..
    Bata, Iqbal
    Dalhousie Univ, Halifax, NS B3H 3J5, Canada..
    Batieha, Anwar M.
    Jordan Univ Sci & Technol, Amman, Jordan..
    Batista, Rosangela L.
    Univ Fed Maranhao, Sao Luis, Brazil..
    Baur, Louise A.
    Univ Sydney, Sydney, NSW 2006, Australia..
    Beaglehole, Robert
    Univ Auckland, Auckland 1, New Zealand..
    Ben Romdhane, Habiba
    Univ Tunis El Manar, Tunis, Tunisia..
    Benet, Mikhail
    Univ Med Sci, Havana, Cuba..
    Bernabe-Ortiz, Antonio
    Univ Peruana Cayetano Heredia, Lima, Peru..
    Bernotiene, Gailute
    Lithuanian Univ Hlth Sci, Kaunas, Lithuania..
    Bettiol, Heloisa
    Univ Sao Paulo, BR-05508 Sao Paulo, Brazil..
    Bhagyalaxmi, Aroor
    BJ Med Coll, New Delhi, India..
    Bharadwaj, Sumit
    Chirayu Med Coll, Bhopal, India..
    Bhargava, Santosh K.
    Sunder Lal Jain Hosp, New Delhi, India..
    Bhatti, Zaid
    Aga Khan Univ, Lahore, Pakistan..
    Bhutta, Zulfiqar A.
    Aga Khan Univ, Lahore, Pakistan..
    Bi, HongSheng
    Shandong Univ Tradit Chinese Med, Jinan, Peoples R China..
    Bi, Yufang
    Shanghai Jiao Tong Univ, Sch Med, Shanghai 200030, Peoples R China..
    Bjerregaard, Peter
    Univ Southern Denmark, Lyngby, Denmark..
    Bjertness, Espen
    Univ Oslo, N-0316 Oslo, Norway..
    Bjertness, Marius B.
    Univ Oslo, N-0316 Oslo, Norway..
    Bjorkelund, Cecilia
    Gothenburg Univ, S-41124 Gothenburg, Sweden..
    Blake, Margaret
    NatCen Social Res, London, England..
    Blokstra, Anneke
    Natl Inst Publ Hlth & Environm, Amsterdam, Netherlands..
    Bo, Simona
    Univ Turin, I-10124 Turin, Italy..
    Bobak, Martin
    UCL, London WC1E 6BT, England..
    Boddy, Lynne M.
    Liverpool John Moores Univ, Liverpool L3 5UX, Merseyside, England..
    Boehm, Bernhard O.
    Nanyang Technol Univ, Singapore 639798, Singapore..
    Boeing, Heiner
    German Inst Human Nutr, Berlin, Germany..
    Boissonnet, Carlos P.
    CEMIC, Buenos Aires, DF, Argentina..
    Bongard, Vanina
    Toulouse Univ, Sch Med, Toulouse, France..
    Bovet, Pascal
    Minist Hlth, Victoria, Seychelles.;Univ Lausanne, CH-1015 Lausanne, Switzerland..
    Braeckman, Lutgart
    Univ Ghent, B-9000 Ghent, Belgium..
    Bragt, Marjolijn C. E.
    FrieslandCampina, Singapore, Singapore..
    Brajkovich, Imperia
    Cent Univ Venezuela, Caracas, Venezuela..
    Branca, Francesco
    WHO, CH-1211 Geneva, Switzerland..
    Breckenkamp, Juergen
    Univ Bielefeld, Bielefeld, Germany..
    Brenner, Hermann
    German Canc Res Ctr, Berlin, Germany..
    Brewster, Lizzy M.
    Univ Amsterdam, NL-1012 WX Amsterdam, Netherlands..
    Brian, Garry R.
    Fred Hollows Fdn New Zealand, Auckland, New Zealand..
    Bruno, Graziella
    Univ Turin, I-10124 Turin, Italy..
    Bueno-de-Mesquita, H. B(as)
    Natl Inst Publ Hlth & Environm, Amsterdam, Netherlands..
    Bugge, Anna
    Univ Southern Denmark, Lyngby, Denmark..
    Burns, Con
    Cork Inst Technol, Cork, Ireland..
    Cabrera de Leon, Antonio
    Univ La Laguna, E-38207 San Cristobal la Laguna, Spain..
    Cacciottolo, Joseph
    Univ Malta, Msida, Malta..
    Cama, Tilema
    Minist Hlth, Nukualofa, Tonga..
    Cameron, Christine
    Canadian Fitness & Lifestyle Res Inst, Toronto, ON, Canada..
    Camolas, Jose
    Hosp Santa Maria, CHLN, Lisbon, Portugal..
    Can, Gunay
    Istanbul Univ, Istanbul, Turkey..
    Candido, Ana Paula C.
    Univ Fed Juiz de Fora, Juiz De Fora, Brazil..
    Capuano, Vincenzo
    Cardiol Mercato S Severino, Mercato San Severino, Italy..
    Cardoso, Viviane C.
    Univ Sao Paulo, BR-05508 Sao Paulo, Brazil..
    Carvalho, Maria J.
    Univ Porto, Rua Campo Alegre 823, P-4100 Oporto, Portugal..
    Casanueva, Felipe F.
    Univ Santiago de Compostela, Santiago De Compostela, Spain..
    Casas, Juan-Pablo
    UCL, London WC1E 6BT, England..
    Caserta, Carmelo A.
    Assoc Calabrese Epatol, Rome, Italy..
    Castetbon, Katia
    French Inst Hlth Surveillance, Lyon, France..
    Chamukuttan, Snehalatha
    India Diabet Res Fdn, New Delhi, India..
    Chan, Angelique W.
    Duke NUS Grad Med Sch, Singapore, Singapore..
    Chan, Queenie
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Chaturvedi, Himanshu K.
    Natl Inst Med Stat, New Delhi, India..
    Chaturvedi, Nishi
    UCL, London WC1E 6BT, England..
    Chen, Chien-Jen
    Acad Sinica, Taipei, Taiwan..
    Chen, Fangfang
    Capital Inst Pediat, Beijing, Peoples R China..
    Chen, Huashuai
    Duke Univ, Durham, NC 27706 USA..
    Chen, Shuohua
    Kailuan Gen Hosp, Beijing, Peoples R China..
    Chen, Zhengming
    Univ Oxford, Oxford OX1 2JD, England..
    Cheng, Ching-Yu
    Duke NUS Grad Med Sch, Singapore, Singapore..
    Chetrit, Angela
    Gertner Inst Epidemiol & Hlth Policy Res, Tel Aviv, Israel..
    Chiolero, Arnaud
    Univ Lausanne Hosp, Lausanne, Switzerland..
    Chiou, Shu-Ti
    Minist Hlth & Welf, Taipei, Taiwan..
    Chirita-Emandi, Adela
    Victor Babes Univ Med & Pharm, Cluj Napoca, Romania..
    Cho, Yumi
    Korea Ctr Dis Control & Prevent, Seoul, South Korea..
    Christensen, Kaare
    Univ Southern Denmark, Lyngby, Denmark..
    Chudek, Jerzy
    Med Univ Silesia, Katowice, Poland..
    Cifkova, Renata
    Charles Univ Prague, Prague, Czech Republic..
    Claessens, Frank
    Katholieke Univ Leuven, Louvain, Belgium..
    Clays, Els
    Univ Ghent, B-9000 Ghent, Belgium..
    Concin, Hans
    Agcy Prevent & Social Med, Vienna, Austria..
    Cooper, Cyrus
    Univ Southampton, Southampton SO9 5NH, Hants, England..
    Cooper, Rachel
    UCL, London WC1E 6BT, England..
    Coppinger, Tara C.
    Cork Inst Technol, Cork, Ireland..
    Costanzo, Simona
    IRCCS Ist Neurol Mediterraneo Neuromed, Rome, Italy..
    Cottel, Dominique
    Inst Pasteur, Lille, France..
    Cowell, Chris
    Westmead Univ Sydney, Sydney, NSW, Australia..
    Craig, Cora L.
    Canadian Fitness & Lifestyle Res Inst, Toronto, ON, Canada..
    Crujeiras, Ana B.
    CIBEROBN, Madrid, Spain..
    D'Arrigo, Graziella
    CNR, Rome, Italy..
    d'Orsi, Eleonora
    Univ Fed Santa Catarina, BR-88040900 Florianopolis, SC, Brazil..
    Dallongeville, Jean
    Inst Pasteur, Lille, France..
    Damasceno, Albertino
    Eduardo Mondlane Univ, Maputo, Mozambique..
    Damsgaard, Camilla T.
    Univ Copenhagen, DK-1168 Copenhagen, Denmark..
    Dankner, Rachel
    Gertner Inst Epidemiol & Hlth Policy Res, Tel Aviv, Israel..
    Dauchet, Luc
    Lille Univ Hosp, Lille, France..
    De Backer, Guy
    Univ Ghent, B-9000 Ghent, Belgium..
    De Bacquer, Dirk
    Univ Ghent, B-9000 Ghent, Belgium..
    de Gaetano, Giovanni
    IRCCS Ist Neurol Mediterraneo Neuromed, Rome, Italy..
    De Henauw, Stefaan
    Univ Ghent, B-9000 Ghent, Belgium..
    De Smedt, Delphine
    Univ Ghent, B-9000 Ghent, Belgium..
    Deepa, Mohan
    Madras Diabet Res Fdn, Madras, Tamil Nadu, India..
    Deev, Alexander D.
    Natl Res Ctr Prevent Med, Moscow, Russia..
    Dehghan, Abbas
    Erasmus MC, Rotterdam, Netherlands.;Univ Amsterdam, Acad Med Ctr, NL-1012 WX Amsterdam, Netherlands..
    Delisle, Helene
    Univ Montreal, Montreal, PQ H3C 3J7, Canada..
    Delpeuch, Francis
    Inst Rech Dev, Lyon, France..
    Dhana, Klodian
    Erasmus MC, Rotterdam, Netherlands..
    Di Castelnuovo, Augusto F.
    IRCCS Ist Neurol Mediterraneo Neuromed, Rome, Italy..
    Dias-da-Costa, Juvenal Soares
    Univ Vale Rio dos Sinos, Sao Leopoldo, RS, Brazil..
    Diaz, Alejandro
    Natl Council Sci & Tech Res, Buenos Aires, DF, Argentina..
    Djalalinia, Shirin
    Noncommunicable Dis Res Ctr, Tehran, Iran..
    Do, Ha T. P.
    Natl Inst Nutr, Hanoi, Vietnam..
    Dobson, Annette J.
    Univ Queensland, Brisbane, Qld 4072, Australia..
    Donfrancesco, Chiara
    Ist Super Sanita, Rome, Italy..
    Doering, Angela
    Helmholtz Zentrum mUNCHEN, Munich, Germany..
    Doua, Kouamelan
    Minist Sante & Lutte Sida, Yamoussoukro, Cote Ivoire..
    Drygas, Wojciech
    Cardinal Wyszynski Inst Cardiol, Warsaw, Poland..
    Egbagbe, Eruke E.
    Univ Benin, Coll Med Sci, Benin, Nigeria..
    Eggertsen, Robert
    Gothenburg Univ, S-41124 Gothenburg, Sweden..
    Ekelund, Ulf
    Norwegian Sch Sport Sci, Oslo, Norway..
    El Ati, Jalila
    Natl Inst Nutr & Food Technol, Tunis, Tunisia..
    Elliott, Paul
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Engle-Stone, Reina
    Univ Calif Davis, Davis, CA USA..
    Erasmus, Rajiv T.
    Univ Stellenbosch, ZA-7600 Stellenbosch, South Africa..
    Erem, Cihangir
    Karadeniz Tech Univ, Trabzon, Turkey..
    Eriksen, Louise
    Univ Southern Denmark, Lyngby, Denmark..
    Escobedo-de la Pena, Jorge
    Inst Mexicano Seguro Social, Rio Grande, Mexico..
    Evans, Alun
    Queens Univ Belfast, Belfast BT7 1NN, Antrim, North Ireland..
    Faeh, David
    Univ Zurich, CH-8006 Zurich, Switzerland..
    Fall, Caroline H.
    Univ Southampton, Southampton SO9 5NH, Hants, England.;Univ Tehran Med Sci, Tehran, Iran..
    Farzadfar, Farshad
    Felix-Redondo, Francisco J.
    Ferguson, Trevor S.
    Univ W Indies, Kingston, Jamaica..
    Fernandez-Berges, Daniel
    Ferrante, Daniel
    Minist Hlth, Buenos Aires, DF, Argentina..
    Ferrari, Marika
    Council Agr Res & Econ, Rome, Italy..
    Ferreccio, Catterina
    Ferrieres, Jean
    Toulouse Univ, Sch Med, Toulouse, France..
    Finn, Joseph D.
    Univ Manchester, Manchester M13 9PL, Lancs, England..
    Fischer, Krista
    Univ Tartu, Tartu, Estonia..
    Monterubio Flores, Eric
    Inst Nacl Salud Publ, Mexico City, DF, Mexico..
    Foeger, Bernhard
    Agcy Prevent & Social Med, Vienna, Austria..
    Foo, Leng Huat
    Univ Sains Malaysia, Shah Alam, Malaysia..
    Forslund, Ann-Sofie
    Univ Lulea, S-97187 Lulea, Sweden..
    Fortmann, Stephen P.
    Stanford Univ, Stanford, CA 94305 USA..
    Fouad, Heba M.
    Francis, Damian K.
    Franco, Maria do Carmo
    Franco, Oscar H.
    Erasmus MC, Rotterdam, Netherlands.;Univ Fed Sao Paulo, Sao Paulo, Brazil..
    Frontera, Guillermo
    Fuchs, Flavio D.
    Fuchs, Sandra C.
    Univ Fed Rio Grande do Sul, BR-90046900 Porto Alegre, RS, Brazil..
    Fujita, Yuki
    Kinki Univ, Fac Med, Higashiosaka, Osaka 577, Japan..
    Furusawa, Takuro
    Kyoto Univ, Kyoto 6068501, Japan..
    Gaciong, Zbigniew
    Med Univ Warsaw, Warsaw, Poland..
    Gafencu, Mihai
    Victor Babes Univ Med & Pharm, Cluj Napoca, Romania..
    Gareta, Dickman
    Garnett, Sarah P.
    Univ Sydney, Sydney, NSW 2006, Australia..
    Gaspoz, Jean-Michel
    Univ Hosp Geneva, Geneva, Switzerland..
    Gasull, Magda
    Gates, Louise
    Geleijnse, Johanna M.
    Wageningen Univ, NL-6700 AP Wageningen, Netherlands..
    Ghasemian, Anoosheh
    Noncommunicable Dis Res Ctr, Tehran, Iran..
    Giampaoli, Simona
    Ist Super Sanita, Rome, Italy..
    Gianfagna, Francesco
    Univ Insubria, Varese, Italy..
    Giovannelli, Jonathan
    Lille Univ Hosp, Lille, France..
    Giwercman, Aleksander
    Lund Univ, S-22100 Lund, Sweden..
    Goldsmith, Rebecca A.
    Gonzalez Gross, Marcela
    Univ Politecn Madrid, E-28040 Madrid, Spain..
    Gonzalez Rivas, Juan P.
    Andes Clin Cardiometab Studies, Caracas, Venezuela..
    Bonet Gorbea, Mariano
    Natl Inst Hyg Epidemiol & Microbiol, Havana, Cuba..
    Gottrand, Frederic
    Univ Lille 2, F-59800 Lille, France..
    -Iversen, Sidsel Graff
    Norwegian Inst Publ Hlth, Oslo, Norway..
    Grafnetter, Dusan
    Inst Clin & Expt Med, Prague, Czech Republic..
    Grajda, Aneta
    Childrens Mem Hlth Inst, Warsaw, Poland..
    Grammatikopoulou, Maria G.
    Alexander Technol Educ Inst, Athens, Greece..
    Gregor, Ronald D.
    Dalhousie Univ, Halifax, NS B3H 3J5, Canada..
    Grodzicki, Tomasz
    Jagiellonian Univ, Coll Med, PL-31007 Krakow, Poland..
    Grontved, Anders
    Univ Southern Denmark, Lyngby, Denmark..
    Gruden, Grabriella
    Univ Turin, I-10124 Turin, Italy..
    Grujic, Vera
    Inst Publ Hlth Vojvodina, Belgrade, Serbia..
    Gu, Dongfeng
    Natl Ctr Cardiovasc Dis, Beijing, Peoples R China..
    Guan, Ong Peng
    Singapore Eye Res Inst, Singapore, Singapore..
    Gudnason, Vilmundur
    Iceland Heart Assoc, Kopavogur, Iceland..
    Guerrero, Ramiro
    Univ Icesi, Cali, Colombia..
    Guessous, Idris
    Univ Hosp Geneva, Geneva, Switzerland..
    Guimaraes, Andre L.
    Gulliford, Martin C.
    Kings Coll London, London WC2R 2LS, England..
    Gunnlaugsdottir, Johanna
    Guo, Xiu H.
    Capital Med Univ, Beijing, Peoples R China..
    Guo, Yin
    Capital Med Univ, Beijing, Peoples R China..
    Gupta, Prakash C.
    Healis Sekhsaria Inst Publ Hlth, New Delhi, India..
    Gureje, Oye
    Univ Ibadan, Ibadan, Nigeria..
    Gurzkowska, Beata
    Childrens Mem Hlth Inst, Warsaw, Poland..
    Gutierrez, Laura
    Inst Clin Effectiveness & Hlth Policy, Buenos Aires, DF, Argentina..
    Gutzwiller, Felix
    Univ Zurich, CH-8006 Zurich, Switzerland..
    Halkjaer, Jytte
    Danish Canc Soc Res Ctr, Lyngby, Denmark..
    Hardy, Rebecca
    UCL, London WC1E 6BT, England..
    Kumar, Rachakulla Hari
    Indian Council Med Res, New Delhi, India..
    Hayes, Alison J.
    Univ Sydney, Sydney, NSW 2006, Australia.;Tulane Univ, New Orleans, LA 70118 USA..
    He, Jiang
    Hendriks, Marleen Elisabeth
    Univ Amsterdam, Acad Med Ctr, NL-1012 WX Amsterdam, Netherlands..
    Hernandez Cadena, Leticia
    Natl Inst Publ Hlth, Mexicali, Baja California, Mexico..
    Heshmat, Ramin
    Hihtaniemi, Ilpo Tapani
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Ho, Sai Yin
    Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China..
    Ho, Suzanne C.
    Chinese Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China..
    Hobbs, Michael
    Univ Western Australia, Nedlands, WA 6009, Australia..
    Hofman, Albert
    Erasmus MC, Rotterdam, Netherlands..
    Hormiga, Claudia M.
    Horta, Bernardo L.
    Univ Fed Pelotas, Pelotas, Brazil..
    Houti, Leila
    Univ Oran 1, Oran, Algeria..
    Htay, Thein Thein
    Htet, Aung Soe
    Univ Oslo, N-0316 Oslo, Norway..
    Htike, Maung Maung Than
    Minist Hlth, Naypyidaw, Myanmar..
    Hu, Yonghua
    Peking Univ, Hlth Sci Ctr, Beijing, Peoples R China..
    Hussieni, Abdullatif S.
    Birzeit Univ, Bir Zayt, Israel..
    Huu, Chinh Nguyen
    Huybrechts, Inge
    Int Agcy Res Canc, Lyon, France..
    Hwalla, Nahla
    Amer Univ Beirut, Beirut, Lebanon..
    Iacoviello, Licia
    IRCCS Ist Neurol Mediterraneo Neuromed, Rome, Italy..
    Iannone, Anna G.
    Cardiol Mercato S Severino, Mercato San Severino, Italy..
    Ibrahim, M. Mohsen
    Cairo Univ, Cairo, Egypt..
    Ikram, M. Arfan
    Erasmus MC, Rotterdam, Netherlands..
    Irazola, Vilma E.
    Islam, Muhammad
    Aga Khan Univ, Lahore, Pakistan..
    Iwasaki, Masanori
    Niigata Univ, Niigata 95021, Japan..
    Jackson, Rod T.
    Univ Auckland, Auckland 1, New Zealand..
    Jacobs, Jeremy M.
    Hadassah Univ, Med Ctr, Tel Aviv, Israel..
    Jafar, Tazeen
    Duke NUS Grad Med Sch, Singapore, Singapore..
    Jamil, Kazi M.
    Kuwait Inst Scientifi c Res, Kuwait, Kuwait..
    Jamrozik, Konrad
    Univ Adelaide, Adelaide, SA 5005, Australia..
    Jasienska, Grazyna
    Jiang, Chao Qiang
    Guangzhou 12th Hosp, Guangzhou, Guangdong, Peoples R China..
    Joffres, Michel
    Simon Fraser Univ, Burnaby, BC V5A 1S6, Canada..
    Johansson, Mattias
    Jonas, Jost B.
    Heidelberg Univ, Heidelberg, Germany..
    Jorgensen, Torben
    Joshi, Pradeep
    World Hlth Org Country Off, New Delhi, India..
    Juolevi, Anne
    Natl Inst Hlth & Welf, Espoo, Finland..
    Jurak, Gregor
    Univ Ljubljana, Ljubljana 61000, Slovenia..
    Juresa, Vesna
    Univ Zagreb, Zagreb 41000, Croatia..
    Kaaks, Rudolf
    German Canc Res Ctr, Berlin, Germany..
    Kafatos, Anthony
    Univ Crete, Iraklion, Greece..
    Kalter-Leibovici, Ofra
    Gertner Inst Epidemiol & Hlth Policy Res, Tel Aviv, Israel..
    Kapantais, Efthymios
    Hellen Med Assoc Obes, Iraklion, Greece..
    Kasaeian, Amir
    Noncommunicable Dis Res Ctr, Tehran, Iran..
    Katz, Joanne
    Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA..
    Kaur, Prabhdeep
    Natl Inst Epidemiol, Madras, Tamil Nadu, India..
    Kavousi, Maryam
    Erasmus MC, Rotterdam, Netherlands..
    Keil, Ulrich
    Univ Munster, Munster, Germany..
    Boker, Lital Keinan
    Univ Haifa, IL-31999 Haifa, Israel..
    Kelishadi, Roya
    Kemper, Han H. C. G.
    Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands..
    Kengne, Andre P.
    South African Med Res Council, Johannesburg, South Africa..
    Kersting, Mathilde
    Res Inst Child Nutr FKE, Munich, Germany..
    Key, Timothy
    Univ Oxford, Oxford OX1 2JD, England..
    Khader, Yousef Saleh
    Jordan Univ Sci & Technol, Amman, Jordan..
    Khalili, Davood
    Shahid Beheshti Univ Med Sci, Tehran, Iran..
    Khaw, Kay-Tee H.
    Univ Cambridge, Cambridge CB2 1TN, England..
    Khouw, Ilse M. S. L.
    FrieslandCampina, Singapore, Singapore..
    Kiechl, Stefan
    Med Univ Innsbruck, A-6020 Innsbruck, Austria..
    Killewo, Japhet
    Univ Hlth & Allied Sci, Tanza, Tanzania..
    Kim, Jeongseon
    Natl Canc Ctr, Seoul, South Korea..
    Kiyohara, Yutaka
    Kyushu Univ, Fukuoka 812, Japan..
    Klimont, Jeannette
    Stat Austria, Vienna, Austria..
    Kolle, Elin
    Norwegian Sch Sport Sci, Oslo, Norway..
    Kolsteren, Patrick
    Inst Trop Med, Brussels, Belgium..
    Korrovits, Paul
    Tartu Univ Clin, Tartu, Estonia..
    Koskinen, Seppo
    Kouda, Katsuyasu
    Kinki Univ, Fac Med, Higashiosaka, Osaka 577, Japan..
    Koziel, Slawomir
    Polish Acad Sci, Anthropol Unit, Wroclaw, Poland..
    Kratzer, Wolfgang
    Univ Hosp Ulm, Ulm, Germany..
    Krokstad, Steinar
    Norwegian Univ Sci & Technol, Oslo, Norway..
    Kromhout, Daan
    Wageningen Univ, NL-6700 AP Wageningen, Netherlands..
    Kruger, Herculina S.
    North West Univ, Johannesburg, South Africa..
    Kula, Krzysztof
    Med Univ Lodz, Lodz, Poland..
    Kulaga, Zbigniew
    Childrens Mem Hlth Inst, Warsaw, Poland..
    Kumar, R. Krishna
    Amrita Inst Med Sci, Kochi, India..
    Kusuma, Yadlapalli S.
    All India Inst Med Sci, New Delhi 110029, India..
    Kuulasmaa, Kari
    Laamiri, Fatima Zahra
    Univ Mohammed V Rabat, Rabat, Morocco..
    Laatikainen, Tiina
    Lachat, Carl
    Univ Ghent, B-9000 Ghent, Belgium..
    Laid, Youcef
    Lam, Tai Hing
    Landrove, Orlando
    Lanska, Vera
    Lappas, Georg
    Sahlgrens Acad, Stockholm, Sweden..
    Laugsand, Lars E.
    Norwegian Univ Sci & Technol, Oslo, Norway..
    Bao, Khanh Le Nguyen
    Le, Tuyen D.
    Natl Inst Nutr, Hanoi, Vietnam..
    Leclercq, Catherine
    Food & Agr Org, Rome, Italy..
    Lee, Jeannette
    Natl Univ Singapore, Singapore 117548, Singapore..
    Lee, Jeonghee
    Natl Canc Ctr, Seoul, South Korea..
    Lehtimaki, Terho
    Tampere Univ Hosp, Tampere, Finland..
    Lekhraj, Rampal
    Univ Putra Malaysia, Serdang 43400, Malaysia..
    Leon-Munoz, Luz M.
    Univ Autonoma Madrid, E-28049 Madrid, Spain..
    Lim, Wei-Yen
    Natl Univ Singapore, Singapore 117548, Singapore..
    Fernanda Lima-Costa, M.
    Fundacao Oswaldo Cruz, Rene Rachou Res Inst, Rio De Janeiro, Brazil..
    Lin, Xu
    Univ Chinese Acad Sci, Beijing, Peoples R China..
    Linneberg, Allan
    Res Ctr Prevent & Hlth, Aalborg, Denmark..
    Lissner, Lauren
    Gothenburg Univ, S-41124 Gothenburg, Sweden..
    Litwin, Mieczyslaw
    Childrens Mem Hlth Inst, Lodz, Poland..
    Liu, Jing
    Capital Med Univ, Beijing Anzhen Hosp, Beijing, Peoples R China..
    Lorbeer, Roberto
    Univ Med Greifswald, Greifswald, Germany..
    Lotufo, Paulo A.
    Univ Sao Paulo, BR-05508 Sao Paulo, Brazil..
    Eugenio Lozano, Jose
    Consejeria Sanidad Junta Castilla & Leon, Leon, Spain..
    Luksiene, Dalia
    Lithuanian Univ Hlth Sci, Kaunas, Lithuania..
    Lundqvist, Annamari
    Natl Inst Hlth & Welf, Tampere, Finland..
    Lunet, Nuno
    Univ Porto, Sch Med, Rua Campo Alegre 823, P-4100 Oporto, Portugal..
    Lytsy, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ma, Guansheng
    Peking Univ, Beijing 100871, Peoples R China..
    Machi, Suka
    Jikei Univ, Sch Med, Tokyo, Japan..
    Maggi, Stefania
    CNR, Pisa, Italy..
    Magliano, Dianna J.
    Baker IDI Heart & Diabet Inst, Melbourne, Vic, Australia..
    Makdisse, Marcia
    Hosp Israelita Albert Einstein, Sao Paulo, Brazil..
    Malekzadeh, Reza
    Univ Tehran Med Sci, Tehran, Iran..
    Malhotra, Rahul
    Duke NUS Grad Med Sch, Singapore, Singapore..
    Rao, Kodavanti Mallikharjuna
    Indian Council Med Res, New Delhi, India..
    Manios, Yannis
    Harokopio Univ Athens, Athens, Greece..
    Mann, Jim I.
    Univ Otago, Otaru, Hokkaido, Japan..
    Manzato, Enzo
    Univ Padua, I-35100 Padua, Italy..
    Margozzini, Paula
    Pontificia Univ Catolica Chile, Santiago, Chile..
    Markey, Oonagh
    Univ Reading, Reading RG6 2AH, Berks, England..
    Marques-Vidal, Pedro
    Univ Lausanne Hosp, Lausanne, Switzerland..
    Marrugat, Jaume
    Martin-Prevel, Yves
    Inst Rech Dev, Lyon, France..
    Martorell, Reynaldo
    Emory Univ, Atlanta, GA 30322 USA..
    Masoodi, Shariq R.
    Sherikashmir Inst Med Sci, Jammu, India..
    Matsha, Tandi E.
    Cape Peninsula Univ Technol, Cape Town, South Africa..
    Mazur, Artur
    Univ Rzeszow, Rzeszow, Poland..
    Mbanya, Jean Claude N.
    Univ Yaounde I, Yaounde, Cameroon..
    McFarlane, Shelly R.
    McGarvey, Stephen T.
    Brown Univ, Providence, RI 02912 USA..
    McKee, Martin
    London Sch Hyg & Trop Med, London, England..
    McLachlan, Stela
    Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland..
    McLean, Rachael M.
    McNulty, Breige A.
    Univ Coll Dublin, Dublin, Ireland..
    Yusof, Safiah Md
    Univ Teknol MARA, Serdang, Malaysia..
    Mediene-Benchekor, Sounnia
    Meirhaeghe, Aline
    Meisinger, Christa
    Helmholtz Zentrum mUNCHEN, Munich, Germany..
    Mendes, Larissa L.
    Univ Fed Juiz de Fora, Juiz De Fora, Brazil..
    Menezes, Ana Maria B.
    Mensink, Gert B. M.
    Robert Koch Inst, Berlin, Germany..
    Meshram, Indrapal I.
    Indian Council Med Res, New Delhi, India..
    Metspalu, Andres
    Univ Tartu, Ulikooli 18, EE-50090 Tartu, Estonia..
    Mi, Jie
    Capital Inst Pediat, Beijing, Peoples R China..
    Michaelsen, Kim F.
    Univ Copenhagen, DK-1168 Copenhagen, Denmark..
    Mikkel, Kairit
    Univ Tartu, Ulikooli 18, EE-50090 Tartu, Estonia..
    Miller, Jody C.
    Francisco Miquel, Juan
    Jaime Miranda, J.
    Univ Peruana Cayetano Heredia, Lima, Peru..
    Misigoj-Durakovic, Marjeta
    Univ Zagreb, Zagreb 41000, Croatia..
    Mohamed, Mostafa K.
    Ain Shams Univ, Cairo, Egypt..
    Mohammad, Kazem
    Univ Tehran Med Sci, Tehran, Iran..
    Mohammadifard, Noushin
    Isfahan Cardiovasc Res Ctr, Esfahan, Iran..
    Mohan, Viswanathan
    Madras Diabet Res Fdn, Madras, Tamil Nadu, India..
    Yusoff, Muhammad Fadhli Mohd
    Minist Hlth, Kuala Lumpur, Malaysia..
    Molbo, Drude
    Univ Copenhagen, DK-1168 Copenhagen, Denmark..
    Moller, Niels C.
    Univ Southern Denmark, Lyngby, Denmark..
    Molnar, Denes
    Univ Pecs, Pecs, Hungary..
    Mondo, Charles K.
    Mulago Hosp, Kampala, Uganda..
    Monterrubio, Eric A.
    Monyeki, Kotsedi Daniel K.
    Univ Limpopo, Limpopo, South Africa..
    Moreira, Leila B.
    Morejon, Alain
    Univ Med Sci, Havana, Cuba..
    Moreno, Luis A.
    Univ Zaragoza, E-50009 Zaragoza, Spain..
    Morgan, Karen
    RCSI Dublin, Dublin, Ireland..
    Mortensen, Erik Lykke
    Univ Copenhagen, DK-1168 Copenhagen, Denmark..
    Moschonis, George
    Harokopio Univ Athens, Athens, Greece..
    Mossakowska, Malgorzata
    Mota, Jorge
    Univ Porto, Rua Campo Alegre 823, P-4100 Oporto, Portugal..
    Motlagh, Mohammad Esmaeel
    Ahvaz Jundishapur Univ Med Sci, Tehran, Iran..
    Motta, Jorge
    Gorgas Mem Inst Publ Hlth, Panama City, Panama..
    Mu, Thet Thet
    Muiesan, Maria Lorenza
    Univ Brescia, I-25121 Brescia, Italy..
    Mueller-Nurasyid, Martina
    Helmholtz Zentrum mUNCHEN, Munich, Germany..
    Murphy, Neil
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Mursu, Jaakko
    Univ Eastern Finland, Joensuu, Finland..
    Murtagh, Elaine M.
    Mary Immaculate Coll, Limerick, Ireland..
    Musa, Kamarul Imran
    Univ Sains Malaysia, Kota Baharu, Malaysia..
    Musil, Vera
    Univ Zagreb, Zagreb 41000, Croatia..
    Nagel, Gabriele
    Univ Ulm, D-89069 Ulm, Germany..
    Nakamura, Harunobu
    Namesna, Jana
    Reg Author Publ Hlth, Banska Bystrica, Slovakia..
    Nang, Ei Ei K.
    Nangia, Vinay B.
    Suraj Eye Inst, Nagpur, Maharashtra, India..
    Nankap, Martin
    Helen Keller Int, Yaounde, Cameroon..
    Narake, Sameer
    Maria Navarrete-Munoz, Eva
    Nenko, Ilona
    Neovius, Martin
    Karolinska Inst, S-10401 Stockholm, Sweden..
    Nervi, Flavio
    Neuhauser, Hannelore K.
    Nguyen, Nguyen D.
    Univ Pharm & Med Ho Chi Minh City, Ho Chi Minh City, Vietnam..
    Nguyen, Quang Ngoc
    Nieto-Martinez, Ramfis E.
    Ning, Guang
    Shanghai Jiao Tong Univ, Sch Med, Shanghai 200030, Peoples R China..
    Ninomiya, Toshiharu
    Nishtar, Sania
    Heartfile, Karachi, Pakistan..
    Noale, Marianna
    Norat, Teresa
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Noto, Davide
    Univ Palermo, I-90133 Palermo, Italy..
    Al Nsour, Mohannad
    Eastern Mediterranean Publ Hlth Network, Amman, Jordan..
    O'Reilly, Dermot
    Ochoa-Aviles, Angelica M.
    Univ Cuenca, Cuenca, Ecuador..
    Oh, Kyungwon
    Korea Ctr Dis Control & Prevent, Seoul, South Korea..
    Olayan, Iman H.
    Kuwait Inst Sci Res, Kuwait, Kuwait..
    Anselmo Olinto, Maria Teresa
    Univ Vale Rio dos Sinos, Sao Leopoldo, RS, Brazil..
    Oltarzewski, Maciej
    Omar, Mohd A.
    Minist Hlth, Kuala Lumpur, Malaysia..
    Ordunez, Pedro
    Pan Amer Hlth Org, El Paso, TX USA..
    Ortiz, Ana P.
    Univ Puerto Rico, San Juan, PR USA..
    Osler, Merete
    Osmond, Clive
    MRC Lifecourse Epidemiol Unit, Southampton, Hants, England..
    Ostojic, Sergej M.
    Univ Novi Sad, Novi Sad 21000, Serbia..
    Otero, Johanna A.
    Overvad, Kim
    Aarhus Univ, DK-8000 Aarhus C, Denmark..
    Paccaud, Fred Michel
    Padez, Cristina
    Univ Coimbra, P-3000 Coimbra, Portugal..
    Pajak, Andrzej
    Palli, Domenico
    Palloni, Alberto
    Univ Madison Wisconsin, Madison, WI USA..
    Palmieri, Luigi
    Ist Super Sanita, Rome, Italy..
    Panda-Jonas, Songhomitra
    Panza, Francesco
    Univ Bari, I-70121 Bari, Italy..
    Parnell, Winsome R.
    Parsaeian, Mahboubeh
    Noncommunicable Dis Res Ctr, Tehran, Iran..
    Pednekar, Mangesh S.
    Peeters, Petra H.
    Univ Med Ctr Utrecht, Utrecht, Netherlands..
    Peixoto, Sergio Viana
    Pereira, Alexandre C.
    Heart Inst InCor, Sao Paulo, Brazil..
    Perez, Cynthia M.
    Peters, Annette
    Helmholtz Zentrum mUNCHEN, Munich, Germany..
    Peykari, Niloofar
    Noncommunicable Dis Res Ctr, Tehran, Iran..
    Pham, Son Thai
    Pigeot, Iris
    Leibniz Inst Prevent Res & Epidemiol BIPS, Leibniz, Germany..
    Pikhart, Hynek
    UCL, London WC1E 6BT, England..
    Pilav, Aida
    Fed Minist Hlth, Sarajevo, Bosnia & Herceg..
    Pilotto, Lorenza
    Pistelli, Francesco
    Univ Hosp Pisa, Pisa, Italy..
    Pitakaka, Freda
    Univ New S Wales, Sydney, NSW 2052, Australia..
    Piwonska, Aleksandra
    Cardinal Wyszynski Inst Cardiol, Warsaw, Poland..
    Piwonski, Jerzy
    Plans-Rubio, Pedro
    Poh, Bee Koon
    Publ Hlth Agcy Catalonia, Catalonia, Spain..
    Porta, Miquel
    Portegies, Marileen L. P.
    Erasmus MC, Rotterdam, Netherlands..
    Poulimeneas, Dimitrios
    Pradeepa, Rajendra
    Madras Diabet Res Fdn, Madras, Tamil Nadu, India..
    Prashant, Mathur
    Indian Council Med Res, New Delhi, India..
    Price, Jacqueline F.
    Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland..
    Puiu, Maria
    Victor Babes Univ Med & Pharm, Cluj Napoca, Romania..
    Punab, Margus
    Tartu Univ Clin, Tartu, Estonia..
    Qasrawi, Radwan F.
    Al Quds Univ, Jerusalem, Israel..
    Qorbani, Mostafa
    Alborz Univ Med Sci, Golestan, Iran..
    Bao, Tran Quoc
    Radic, Ivana
    Inst Publ Hlth Vojvodina, Vojvodina, Serbia..
    Radisauskas, Ricardas
    Lithuanian Univ Hlth Sci, Kaunas, Lithuania..
    Rahman, Mahmudur
    Inst Epidemiol Dis Control & Res, Dhaka, Bangladesh..
    Raitakari, Olli
    Turku Univ Hosp, FIN-20520 Turku, Finland..
    Raj, Manu
    Rao, Sudha Ramachandra
    Ramachandran, Ambady
    India Diabet Res Fdn, New Delhi, India..
    Ramke, Jacqueline
    Univ New S Wales, Sydney, NSW 2052, Australia..
    Ramos, Rafel
    Rampal, Sanjay
    Univ Malaya, Serdang, Malaysia..
    Rasmussen, Finn
    Redon, Josep
    Univ Valencia, E-46003 Valencia, Spain..
    Reganit, Paul Ferdinand M.
    Univ Philippines, Quezon City 1101, Philippines..
    Ribeiro, Robespierre
    Riboli, Elio
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Rigo, Fernando
    Hlth Ctr San Agustin, Madrid, Spain..
    de Wit, Tobias Floris Rinke
    PharmAccess Fdn, Groningen, Netherlands..
    Ritti-Dias, Raphael M.
    Rivera, Juan A.
    Robinson, Sian M.
    Univ Southampton, Southampton SO9 5NH, Hants, England..
    Robitaille, Cynthia
    Publ Hlth Agcy Canada, Montreal, PQ, Canada..
    Rodriguez-Artalejo, Fernando
    Univ Autonoma Madrid, E-28049 Madrid, Spain..
    del Cristo Rodriguez-Perez, Maria
    Canarian Hlth Serv, Madrid, Spain..
    Rodriguez-Villamizar, Laura A.
    Univ Ind Santander, Santander, Colombia..
    Rojas-Martinez, Rosalba
    Rojroongwasinkul, Nipa
    Mahidol Univ, Bangkok 10700, Thailand..
    Romaguera, Dora
    CIBEROBN, Madrid, Spain..
    Ronkainen, Kimmo
    Rosengren, Annika
    Gothenburg Univ, S-41124 Gothenburg, Sweden..
    Rouse, Ian
    Fiji Natl Univ, Nasinu, Fiji..
    Rubinstein, Adolfo
    Inst Clin Effectiveness & Hlth Policy, Buenos Aires, DF, Argentina..
    Ruehli, Frank J.
    Univ Zurich, CH-8006 Zurich, Switzerland..
    Rui, Ornelas
    Univ Madeira, Funchal, Portugal..
    Sandra Ruiz-Betancourt, Blanca
    Inst Mexicano Seguro Social, Rio Grande, Mexico..
    Russo Horimoto, Andrea R. V.
    Rutkowski, Marcin
    Med Univ Gdansk, Gdansk, Poland..
    Sabanayagam, Charumathi
    Singapore Eye Res Inst, Singapore, Singapore..
    Sachdev, Harshpal S.
    Sitaram Bhartia Inst Sci & Res, New Delhi, India..
    Saidi, Olfa
    Fac Med Tunis, Tunis, Tunisia..
    Salanave, Benoit
    French Inst Hlth Surveillance, Lyon, France..
    Salazar Martinez, Eduardo
    Salomaa, Veikko
    Salonen, Jukka T.
    Univ Helsinki, FIN-00014 Helsinki, Finland..
    Salvetti, Massimo
    Univ Brescia, I-25121 Brescia, Italy..
    Sanchez-Abanto, Jose
    Natl Inst Hlth, Lima, Peru..
    Sandjaja,
    Sans, Susana
    Catalan Dept Hlth, Madrid, Spain..
    Santos, Diana A.
    Univ Lisbon, P-1699 Lisbon, Portugal..
    Santos, Osvaldo
    dos Santos, Renata Nunes
    Univ Sao Paulo, BR-05508 Sao Paulo, Brazil..
    Santos, Rute
    Univ Porto, Rua Campo Alegre 823, P-4100 Oporto, Portugal..
    Sardinha, Luis B.
    Univ Lisbon, P-1699 Lisbon, Portugal..
    Sarrafzadegan, Nizal
    Saum, Kai-Uwe
    German Canc Res Ctr, Berlin, Germany..
    Savva, Savvas C.
    Res & Educ Inst Child Hlth, Nicosia, Cyprus..
    Scazufca, Marcia
    Univ Sao Paulo, BR-05508 Sao Paulo, Brazil..
    Rosario, Angelika Schaffrath
    Schargrodsky, Herman
    Hosp Italiano Buenos Aires, Buenos Aires, DF, Argentina..
    Schienkiewitz, Anja
    Schmidt, Ida Maria
    Rigshosp, Copenhagen, Denmark..
    Schneider, Ione J.
    Univ Fed Santa Catarina, BR-88040900 Florianopolis, SC, Brazil..
    Schultsz, Constance
    Univ Amsterdam, Acad Med Ctr, NL-1012 WX Amsterdam, Netherlands..
    Schutte, Aletta E.
    MRC North West Univ, Johannesburg, South Africa..
    Sein, Aye Aye
    Minist Hlth, Bangkok, Thailand..
    Senbanjo, Idowu O.
    Lagos State Univ, Coll Med, Lagos, Nigeria..
    Sepanlou, Sadaf G.
    Digest Dis Res Inst, Tehran, Iran..
    Shalnova, Svetlana A.
    Natl Res Ctr Prevent Med, Moscow, Russia..
    Shaw, Jonathan E.
    Shibuya, Kenji
    Univ Tokyo, Tokyo 1138654, Japan..
    Shin, Youchan
    Shiri, Rahman
    Finnish Inst Occupat Hlth, Espoo, Finland..
    Siantar, Rosalynn
    Sibai, Abla M.
    Silva, Antonio M.
    Univ Fed Maranhao, Sao Luis, Brazil.;Univ Fed Santa Catarina, BR-88040900 Florianopolis, SC, Brazil..
    Santos Silva, Diego Augusto
    Simon, Mary
    India Diabet Res Fdn, New Delhi, India..
    Simons, Judith
    St Vincents Hosp, Melbourne, Vic, Australia..
    Simons, Leon A.
    Sjostrom, Michael
    Slowikowska-Hilczer, Jolanta
    Med Univ Lodz, Lodz, Poland..
    Slusarczyk, Przemyslaw
    Smeeth, Liam
    London Sch Hyg & Trop Med, London, England..
    Smith, Margaret C.
    Univ Oxford, Oxford OX1 2JD, England..
    Snijder, Marieke B.
    So, Hung-Kwan
    Chinese Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China..
    Sobngwi, Eugene
    Univ Yaounde I, Yaounde, Cameroon..
    Soderberg, Stefan
    Umea Univ, S-90187 Umea, Sweden..
    Soekatri, Moesijanti Y. E.
    Hlth Polytech Inst, Bandung, Indonesia..
    Solfrizzi, Vincenzo
    Univ Bari, I-70121 Bari, Italy..
    Sonestedt, Emily
    Lund Univ, S-22100 Lund, Sweden..
    Sorensen, Thorkild I. A.
    Univ Copenhagen, DK-1168 Copenhagen, Denmark..
    Soric, Maroje
    Univ Zagreb, Zagreb 41000, Croatia..
    Jerome, Charles Sossa
    Soumare, Aicha
    Univ Bordeaux, Bordeaux, France..
    Staessen, Jan A.
    Univ Leuven, Leuven, Belgium..
    Starc, Gregor
    Stathopoulou, Maria G.
    INSERM, F-75654 Paris 13, France..
    Staub, Kaspar
    Univ Zurich, CH-8006 Zurich, Switzerland..
    Stavreski, Bill
    Heart Fdn, Sydney, NSW, Australia..
    Steene-Johannessen, Jostein
    Norwegian Sch Sport Sci, Oslo, Norway..
    Stehle, Peter
    Univ Bonn, Bonn, Germany..
    Stein, Aryeh D.
    Emory Univ, Atlanta, GA 30322 USA..
    Stergiou, George S.
    Sotiria Hosp, Athina, Greece..
    Stessman, Jochanan
    Stieber, Jutta
    Helmholtz Zentrum mUNCHEN, Munich, Germany..
    Stoeckl, Doris
    Helmholtz Zentrum mUNCHEN, Munich, Germany..
    Stocks, Tanja
    Stokwiszewski, Jakub
    Natl Inst Hyg, Natl Inst Publ Hlth, Warsaw, Poland..
    Stratton, Gareth
    Swansea Univ, Swansea, W Glam, Wales..
    Strufaldi, Maria Wany
    Sun, Chien-An
    Fu Jen Catholic Univ, Taipei, Taiwan..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Sung, Yn-Tz
    Chinese Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China..
    Sunyer, Jordi
    Ctr Res Environm Epidemiol, Madrid, Spain..
    Suriyawongpaisal, Paibul
    Mahidol Univ, Bangkok 10700, Thailand..
    Swinburn, Boyd A.
    Univ Auckland, Auckland 1, New Zealand..
    Sy, Rody G.
    Univ Philippines, Quezon City 1101, Philippines..
    Szponar, Lucjan
    Natl Food & Nutr Inst, Warsaw, Poland..
    Tai, E. Shyong
    Natl Univ Singapore, Singapore 117548, Singapore..
    Tammesoo, Mari-Liis
    Univ Tartu, Ulikooli 18, EE-50090 Tartu, Estonia..
    Tamosiunas, Abdonas
    Lithuanian Univ Hlth Sci, Kaunas, Lithuania..
    Tang, Line
    Res Ctr Prevent & Hlth, Odense, Denmark..
    Tang, Xun
    Peking Univ, Hlth Sci Ctr, Beijing 100871, Peoples R China..
    Tanser, Frank
    Univ KwaZulu Natal, Durban, South Africa..
    Tao, Yong
    Peking Univ, Beijing 100871, Peoples R China..
    Tarp, Jakob
    Univ Southern Denmark, Lyngby, Denmark..
    Tarqui-Mamani, Carolina B.
    Natl Inst Hlth, Lima, Peru..
    Taylor, Anne
    Univ Adelaide, Adelaide, SA 5005, Australia..
    Tchibindat, Felicite
    UNICEF, Yaounde, Cameroon..
    Thijs, Lutgarde
    Thuesen, Betina H.
    Tjonneland, Anne
    Danish Canc Soc Res Ctr, Odense, Denmark..
    Tolonen, Hanna K.
    Tolstrup, Janne S.
    Univ Southern Denmark, Lyngby, Denmark..
    Topbas, Murat
    Karadeniz Tech Univ, Ankara, Turkey..
    Topor-Madry, Roman
    Jagiellonian Univ, Coll Med, PL-31007 Krakow, Poland..
    Torrent, Maties
    Traissac, Pierre
    Inst Rech Dev, Lyon, France..
    Trichopoulou, Antonia
    Trichopoulos, Dimitrios
    Harvard Univ, TH Chan Sch Publ Hlth, Boston, MA 02115 USA.;Alexander Technol Educ Inst, Athens, Greece..
    Trinh, Oanh T. H.
    Trivedi, Atul
    Govt Med Coll, New Delhi, India..
    Tshepo, Lechaba
    Sefako Makgatho Hlth Sci Univ, Johannesburg, South Africa..
    Tulloch-Reid, Marshall K.
    Tuomainen, Tomi-Pekka
    Tuomilehto, Jaakko
    Dasman Diabet Inst, Kuwait, Kuwait. Minist Hlth, Hamilton, New Zealand..
    Tynelius, Per
    Karolinska Inst, S-10401 Stockholm, Sweden..
    Tzotzas, Themistoklis
    Hellen Med Assoc Obes, Athens, Greece..
    Tzourio, Christophe
    Univ Bordeaux, Bordeaux, France..
    Ueda, Peter
    Harvard Univ, TH Chan Sch Publ Hlth, Boston, MA 02115 USA..
    Ukoli, Flora A. M.
    Meharry Med Coll, Nashville, TN USA..
    Ulmer, Hanno
    Med Univ Innsbruck, A-6020 Innsbruck, Austria..
    Unal, Belgin
    Dokuz Eylul Univ, TR-35210 Alsancak, Turkey..
    Valdivia, Gonzalo
    Vale, Susana
    Univ Porto, Rua Campo Alegre 823, P-4100 Oporto, Portugal..
    Valvi, Damaskini
    Harvard Univ, TH Chan Sch Publ Hlth, Boston, MA 02115 USA..
    van der Schouw, Yvonne T.
    Univ Med Ctr Utrecht, Utrecht, Netherlands..
    Van Herck, Koen
    Univ Ghent, B-9000 Ghent, Belgium..
    Minh, Hoang Van
    van Valkengoed, Irene G. M.
    Univ Amsterdam, Acad Med Ctr, NL-1012 WX Amsterdam, Netherlands..
    Vanderschueren, Dirk
    Katholieke Univ Leuven, Louvain, Belgium..
    Vanuzzo, Diego
    Ctr Prevenz Cardiovasc Udine, Udine, Italy..
    Vatten, Lars
    Vega, Tomas
    Velasquez-Melendez, Gustavo
    Univ Fed Minas Gerais, Belo Horizonte, MG, Brazil..
    Veronesi, Giovanni
    Univ Insubria, Varese, Italy..
    Verschuren, W. M. Monique
    Natl Inst Publ Hlth & Environm, Amsterdam, Netherlands..
    Viegi, Giovanni
    Viet, Lucie
    Natl Inst Publ Hlth & Environm, Amsterdam, Netherlands..
    Viikari-Juntura, Eira
    Finnish Inst Occupat Hlth, Helsinki, Finland..
    Vineis, Paolo
    Univ London Imperial Coll Sci Technol & Med, London, England..
    Vioque, Jesus
    Univ Miguel Hernandez, Madrid, Spain..
    Virtanen, Jyrki K.
    Visvikis-Siest, Sophie
    INSERM, F-75654 Paris 13, France..
    Viswanathan, Bharathi
    Minist Hlth, Victoria, Seychelles..
    Vollenweider, Peter
    Univ Lausanne Hosp, Lausanne, Switzerland..
    Voutilainen, Sari
    Vrijheid, Martine
    Ctr Res Environm Epidemiol, Madrid, Spain..
    Wade, Alisha N.
    Univ Witwatersrand, ZA-2050 Johannesburg, South Africa..
    Wagner, Aline
    Univ Strasbourg, Strasbourg, France..
    Walton, Janette
    Univ Coll Cork, Cork, Ireland..
    Mohamud, Wan Nazaimoon Wan
    Inst Med Res, Serdang, Malaysia..
    Wang, Ming-Dong
    Wang, Qian
    Xinjiang Med Univ, Xinjiang, Peoples R China..
    Wang, Ya Xing
    Beijing Tongren Hosp, Beijing, Peoples R China..
    Wannamethee, S. Goya
    UCL, London WC1E 6BT, England..
    Wareham, Nicholas
    Univ Cambridge, Cambridge CB2 1TN, England..
    Weerasekera, Deepa
    Minist Hlth, Hamilton, New Zealand..
    Whincup, Peter H.
    Univ London, London WC1E 7HU, England..
    Widhalm, Kurt
    Med Univ Vienna, Vienna, Austria..
    Widyahening, Indah S.
    Univ Indonesia, Bandung, Indonesia..
    Wiecek, Andrzej
    Med Univ Silesia, Katowice, Poland..
    Wilks, Rainford J.
    Willeit, Johann
    Med Univ Innsbruck, A-6020 Innsbruck, Austria..
    Wojtyniak, Bogdan
    Wong, Jyh Eiin
    Univ Kebangsaan Malaysia, Bangi 43600, Malaysia..
    Wong, Tien Yin
    Duke NUS Grad Med Sch, Singapore, Singapore..
    Woo, Jean
    Chinese Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China..
    Woodward, Mark
    Univ Sydney, Sydney, NSW 2006, Australia.;Univ Oxford, Oxford OX1 2JD, England..
    Wu, Frederick C.
    Univ Manchester, Manchester M13 9PL, Lancs, England..
    Wu, JianFeng
    Shandong Univ Tradit Chinese Med, Jinan, Peoples R China..
    Wu, Shou Ling
    Kailuan Gen Hosp, Beijing, Peoples R China..
    Xu, Haiquan
    Minist Agr, Inst Food & Nutr Dev, Beijing, Peoples R China..
    Xu, Liang
    Capital Med Univ, Beijing, Peoples R China..
    Yamborisut, Uruwan
    Mahidol Univ, Bangkok 10700, Thailand..
    Yan, Weili
    Fudan Univ, Shanghai, Peoples R China..
    Yang, Xiaoguang
    Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China..
    Yardim, Nazan
    Minist Hlth, Ankara, Turkey..
    Ye, Xingwang
    Univ Chinese Acad Sci, Beijing, Peoples R China..
    Yiallouros, Panayiotis K.
    Cyprus Univ Technol, Limassol, Cyprus..
    Yoshihara, Akihiro
    Niigata Univ, Niigata 95021, Japan..
    You, Qi Sheng
    Younger-Coleman, Novie O.
    Yusoff, Ahmad F.
    Minist Hlth, Kuala Lumpur, Malaysia..
    Zainuddin, Ahmad A.
    Univ Teknol MARA, Serdang, Malaysia..
    Zambon, Sabina
    Univ Padua, I-35100 Padua, Italy..
    Zdrojewski, Tomasz
    Med Univ Gdansk, Gdansk, Poland..
    Zeng, Yi
    Duke Univ, Durham, NC 27706 USA.;Peking Univ, Beijing 100871, Peoples R China..
    Zhao, Dong
    Capital Med Univ, Beijing Anzhen Hosp, Beijing, Peoples R China..
    Zhao, Wenhua
    Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China..
    Zheng, Yingfeng
    Singapore Eye Res Inst, Singapore, Singapore..
    Zhou, Maigeng
    Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China..
    Zhu, Dan
    Inner Mongolia Med Univ, Inner Mongolia, Peoples R China..
    Zimmermann, Esther
    Bispebjerg Hosp, Copenhagen, Denmark.;Frederiksberg Univ Hosp, Frederiksberg, Denmark..
    Zuniga Cisneros, Julio
    Gorgas Mem Inst Publ Hlth, Panama City, Panama..
    Trends in adult body-mass index in 200 countries from 1975 to 2014: a pooled analysis of 1698 population-based measurement studies with 19.2 million participants2016Inngår i: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 387, nr 10026, s. 1377-1396Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background Underweight and severe and morbid obesity are associated with highly elevated risks of adverse health outcomes. We estimated trends in mean body-mass index (BMI), which characterises its population distribution, and in the prevalences of a complete set of BMI categories for adults in all countries.

    Methods We analysed, with use of a consistent protocol, population-based studies that had measured height and weight in adults aged 18 years and older. We applied a Bayesian hierarchical model to these data to estimate trends from 1975 to 2014 in mean BMI and in the prevalences of BMI categories (<18.5 kg/m(2) [underweight], 18.5 kg/m(2) to <20 kg/m(2), 20 kg/m(2) to <25 kg/m(2), 25 kg/m(2) to <30 kg/m(2), 30 kg/m(2) to <35 kg/m(2), 35 kg/m(2) to <40 kg/m(2), = 40 kg/m(2) [morbid obesity]), by sex in 200 countries and territories, organised in 21 regions. We calculated the posterior probability of meeting the target of halting by 2025 the rise in obesity at its 2010 levels, if post-2000 trends continue.

    Findings We used 1698 population-based data sources, with more than 19.2 million adult participants (9.9 million men and 9.3 million women) in 186 of 200 countries for which estimates were made. Global age-standardised mean BMI increased from 21.7 kg/m(2) (95% credible interval 21.3-22.1) in 1975 to 24.2 kg/m(2) (24.0-24.4) in 2014 in men, and from 22.1 kg/m(2) (21.7-22.5) in 1975 to 24.4 kg/m(2) (24.2-24.6) in 2014 in women. Regional mean BMIs in 2014 for men ranged from 21.4 kg/m(2) in central Africa and south Asia to 29.2 kg/m(2) (28.6-29.8) in Polynesia and Micronesia; for women the range was from 21.8 kg/m(2) (21.4-22.3) in south Asia to 32.2 kg/m(2) (31.5-32.8) in Polynesia and Micronesia. Over these four decades, age-standardised global prevalence of underweight decreased from 13.8% (10.5-17.4) to 8.8% (7.4-10.3) in men and from 14.6% (11.6-17.9) to 9.7% (8.3-11.1) in women. South Asia had the highest prevalence of underweight in 2014, 23.4% (17.8-29.2) in men and 24.0% (18.9-29.3) in women. Age-standardised prevalence of obesity increased from 3.2% (2.4-4.1) in 1975 to 10.8% (9.7-12.0) in 2014 in men, and from 6.4% (5.1-7.8) to 14.9% (13.6-16.1) in women. 2.3% (2.0-2.7) of the world's men and 5.0% (4.4-5.6) of women were severely obese (ie, have BMI = 35 kg/m(2)). Globally, prevalence of morbid obesity was 0.64% (0.46-0.86) in men and 1.6% (1.3-1.9) in women.

    Interpretation If post-2000 trends continue, the probability of meeting the global obesity target is virtually zero. Rather, if these trends continue, by 2025, global obesity prevalence will reach 18% in men and surpass 21% in women; severe obesity will surpass 6% in men and 9% in women. Nonetheless, underweight remains prevalent in the world's poorest regions, especially in south Asia.

  • 70.
    Dumanski, Jan P.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Medicinsk genetik och genomik. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Faculty of Pharmacy, Medical University of Gdansk, Poland.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk epidemiologi.
    Forsberg, Lars A.
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Medicinsk genetik och genomik. Beijer Laboratory of Genome Research, Uppsala University.
    Loss of Chromosome Y in Leukocytes and Major Cardiovascular Events2017Inngår i: Circulation: Cardiovascular Genetics, ISSN 1942-325X, E-ISSN 1942-3268, Vol. 10, nr 4Artikkel i tidsskrift (Annet vitenskapelig)
  • 71.
    Eggers, Kai M
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Kempf, Tibor
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Wallentin, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Wollert, Kai C
    Siegbahn, Agneta
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk kemi.
    Relations of growth-differentiation factor-15 to biomarkers reflecting vascular pathologies in a population-based sample of elderly subjects2012Inngår i: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686, Vol. 72, nr 1, s. 45-51Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background.

    Growth-differentiation factor-15 (GDF-15) has recently emerged as a risk predictor in patients with cardiac diseases. GDF-15 is commonly related to cardiovascular risk factors, inflammatory activity and cardiac abnormalities. However, it is not clear whether it might be an indicator of vascular pathologies as well.

    Methods.

    Circulating levels of GDF-15 were measured in 1004 elderly community dwellers participating in the PIVUS study. The relations of GDF-15 to biomarkers of endothelial activation (E-selectin, P-selectin, ICAM-1, VCAM-1), extracellular matrix degradation (MMP-9, TIMP-1), coagulatory activity (D-dimer, von Willebrand factor, prothrombin fragment 1 + 2, factor VIIa), and fibrinolytic activity (PAI-1 activity, tPA-antigen) were assessed by multiple linear regressions.

    Results.

    The median GDF-15 level was 1135 ng/L. By linear correlation analysis, GDF-15 exhibited a moderate relation to von Willebrand factor (r = 0.30), and weak, albeit significant relations (r = 0.13-0.29) to E-selectin, P-selectin, ICAM-1, VCAM-1, MMP-9, TIMP-1, D-dimer, PAI-1 activity and tPA-antigen. The relations to the assessed biomarkers of endothelial activation, TIMP-1, D-dimer and von Willebrand factor remained significant applying multiple linear regression models adjusted for clinical covariates and echocardiographic data. There were no significant relations between GDF-15 and biomarkers solely reflecting coagulatory activity.

    Conclusions.

    In the elderly, GDF-15 reflects endothelial activation and vascular inflammation and thus, multiple pathways involved in the development and progression of atherosclerosis.

  • 72. Elfstrom, P.
    et al.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Ludvigsson, J. F.
    Systematic review with meta-analysis: associations between coeliac disease and type 1 diabetes2014Inngår i: Alimentary Pharmacology and Therapeutics, ISSN 0269-2813, E-ISSN 1365-2036, Vol. 40, nr 10, s. 1123-1132Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    BackgroundIn the past decade, a number of population-based studies have examined the prevalence of coeliac disease in individuals with type 1 diabetes but prevalences have differed considerably. AimTo examine the prevalence of coeliac disease in individuals with type 1 diabetes. MethodsA systematic review of English-language articles published in PubMed Medline between 2000 and May 2014. Search terms included celiac disease' or coeliac disease' and diabetes mellitus'. Studies were selected with at least 100 individuals with type 1 diabetes being screened for coeliac disease where the coeliac diagnosis was later confirmed through small intestinal biopsy. Data synthesis used random-effects inverse variance-weighted models, and metaregression was used to examine heterogeneity in subgroups. ResultsA pooled analysis, based on 26,605 patients with type 1 diabetes, found a prevalence of biopsy-confirmed coeliac disease of 6.0% (95% CI=5.0-6.9%). Heterogeneity was large (I-2=93.2%). The prevalence was lower in adults with type 1 diabetes (2.7%), and in mixed populations with both children and adults with type 1 diabetes (4.7%) than in children (6.2%) with type 1 diabetes (P<0.001). Additional subgroup analyses could not explain the large variation in coeliac disease prevalence between studies. ConclusionMore than one in twenty patients with type 1 diabetes have biopsy-verified coeliac disease. This prevalence is high enough to motivate screening for coeliac disease among patients with type 1 diabetes.

  • 73.
    Emilsson, Louise
    et al.
    Vardcentralen Varmlands Nysater, Primary Care Res Unit, Varmland County, Sweden.;Univ Oslo, Inst Hlth & Soc, Dept Hlth Management & Hlth Econ, Oslo, Norway..
    Lebwohl, Benjamin
    Columbia Univ Coll Phys & Surg, Dept Med, Celiac Dis Ctr, New York, NY 10032 USA.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Ludvigsson, Jonas F.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Orebro Univ Hosp, Dept Pediat, Orebro, Sweden..
    Cardiovascular disease in patients with coeliac disease: A systematic review and meta-analysis2015Inngår i: Digestive and Liver Disease, ISSN 1590-8658, E-ISSN 1878-3562, Vol. 47, nr 10, s. 847-852Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Coeliac disease has been associated with an increased risk of cardiovascular disease in some studies, whereas other studies have shown no association. We performed a systematic review and meta-analysis of cardiovascular disease in celiac disease. Methods: Pubmed, Cinahl, EMBASE and Medline via Ovid were searched for relevant articles published until January 5, 2015. English-language articles on studies with more than 20 patients were included, and were quality rated using the GRADE risk of bias tool. We used random-effects models and assessed heterogeneity using the I-2 statistic. Results: Ten studies were relevant, reporting the risk of myocardial infarction, cardiovascular death and stroke in 33,128/32,903/32,466 coeliac disease patients respectively. Only one study examined celiac disease and a composite measure of cardiovascular disease and this study found a hazard ratio of 1.10 (95% CI 1.03-1.28). In a meta-analysis, we observed an increased risk of stroke (OR 1.11; 95% CI 1.02-1.20). The risks of myocardial infarction (OR 1.12; 95% CI 0.83-1.40) and cardiovascular death (OR 1.12; 95% CI 0.96-1.29) were similar but were estimated with less certainty. Heterogeneity was low for all outcomes except for myocardial infarction where it was moderate. Conclusion: Coeliac disease was associated with a modestly increased risk of cardiovascular disease, but the evidence base is limited.

  • 74. Evangelou, Evangelos
    et al.
    Warren, Helen R
    Mosen-Ansorena, David
    Mifsud, Borbala
    Pazoki, Raha
    Gao, He
    Ntritsos, Georgios
    Dimou, Niki
    Cabrera, Claudia P
    Karaman, Ibrahim
    Ng, Fu Liang
    Evangelou, Marina
    Witkowska, Katarzyna
    Tzanis, Evan
    Hellwege, Jacklyn N
    Giri, Ayush
    Velez Edwards, Digna R
    Sun, Yan V
    Cho, Kelly
    Gaziano, J Michael
    Wilson, Peter W F
    Tsao, Philip S
    Kovesdy, Csaba P
    Esko, Tonu
    Mägi, Reedik
    Milani, Lili
    Almgren, Peter
    Boutin, Thibaud
    Debette, Stéphanie
    Ding, Jun
    Giulianini, Franco
    Holliday, Elizabeth G
    Jackson, Anne U
    Li-Gao, Ruifang
    Lin, Wei-Yu
    Luan, Jian'an
    Mangino, Massimo
    Oldmeadow, Christopher
    Prins, Bram Peter
    Qian, Yong
    Sargurupremraj, Muralidharan
    Shah, Nabi
    Surendran, Praveen
    Thériault, Sébastien
    Verweij, Niek
    Willems, Sara M
    Zhao, Jing-Hua
    Amouyel, Philippe
    Connell, John
    de Mutsert, Renée
    Doney, Alex S F
    Farrall, Martin
    Menni, Cristina
    Morris, Andrew D
    Noordam, Raymond
    Paré, Guillaume
    Poulter, Neil R
    Shields, Denis C
    Stanton, Alice
    Thom, Simon
    Abecasis, Gonçalo
    Amin, Najaf
    Arking, Dan E
    Ayers, Kristin L
    Barbieri, Caterina M
    Batini, Chiara
    Bis, Joshua C
    Blake, Tineka
    Bochud, Murielle
    Boehnke, Michael
    Boerwinkle, Eric
    Boomsma, Dorret I
    Bottinger, Erwin P
    Braund, Peter S
    Brumat, Marco
    Campbell, Archie
    Campbell, Harry
    Chakravarti, Aravinda
    Chambers, John C
    Chauhan, Ganesh
    Ciullo, Marina
    Cocca, Massimiliano
    Collins, Francis
    Cordell, Heather J
    Davies, Gail
    de Borst, Martin H
    de Geus, Eco J
    Deary, Ian J
    Deelen, Joris
    Del Greco M, Fabiola
    Demirkale, Cumhur Yusuf
    Dörr, Marcus
    Ehret, Georg B
    Elosua, Roberto
    Enroth, Stefan
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi.
    Erzurumluoglu, A Mesut
    Ferreira, Teresa
    Frånberg, Mattias
    Franco, Oscar H
    Gandin, Ilaria
    Gasparini, Paolo
    Giedraitis, Vilmantas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Gieger, Christian
    Girotto, Giorgia
    Goel, Anuj
    Gow, Alan J
    Gudnason, Vilmundur
    Guo, Xiuqing
    Gyllensten, Ulf B.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Hamsten, Anders
    Harris, Tamara B
    Harris, Sarah E
    Hartman, Catharina A
    Havulinna, Aki S
    Hicks, Andrew A
    Hofer, Edith
    Hofman, Albert
    Hottenga, Jouke-Jan
    Huffman, Jennifer E
    Hwang, Shih-Jen
    Ingelsson, Erik
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    James, Alan
    Jansen, Rick
    Jarvelin, Marjo-Riitta
    Joehanes, Roby
    Johansson, Åsa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Johnson, Andrew D
    Joshi, Peter K
    Jousilahti, Pekka
    Jukema, J Wouter
    Jula, Antti
    Kähönen, Mika
    Kathiresan, Sekar
    Keavney, Bernard D
    Khaw, Kay-Tee
    Knekt, Paul
    Knight, Joanne
    Kolcic, Ivana
    Kooner, Jaspal S
    Koskinen, Seppo
    Kristiansson, Kati
    Kutalik, Zoltan
    Laan, Maris
    Larson, Marty
    Launer, Lenore J
    Lehne, Benjamin
    Lehtimäki, Terho
    Liewald, David C M
    Lin, Li
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Lindgren, Cecilia M
    Liu, YongMei
    Loos, Ruth J F
    Lopez, Lorna M
    Lu, Yingchang
    Lyytikäinen, Leo-Pekka
    Mahajan, Anubha
    Mamasoula, Chrysovalanto
    Marrugat, Jaume
    Marten, Jonathan
    Milaneschi, Yuri
    Morgan, Anna
    Morris, Andrew P
    Morrison, Alanna C
    Munson, Peter J
    Nalls, Mike A
    Nandakumar, Priyanka
    Nelson, Christopher P
    Niiranen, Teemu
    Nolte, Ilja M
    Nutile, Teresa
    Oldehinkel, Albertine J
    Oostra, Ben A
    O'Reilly, Paul F
    Org, Elin
    Padmanabhan, Sandosh
    Palmas, Walter
    Palotie, Aarno
    Pattie, Alison
    Penninx, Brenda W J H
    Perola, Markus
    Peters, Annette
    Polasek, Ozren
    Pramstaller, Peter P
    Nguyen, Quang Tri
    Raitakari, Olli T
    Ren, Meixia
    Rettig, Rainer
    Rice, Kenneth
    Ridker, Paul M
    Ried, Janina S
    Riese, Harriëtte
    Ripatti, Samuli
    Robino, Antonietta
    Rose, Lynda M
    Rotter, Jerome I
    Rudan, Igor
    Ruggiero, Daniela
    Saba, Yasaman
    Sala, Cinzia F
    Salomaa, Veikko
    Samani, Nilesh J
    Sarin, Antti-Pekka
    Schmidt, Reinhold
    Schmidt, Helena
    Shrine, Nick
    Siscovick, David
    Smith, Albert V
    Snieder, Harold
    Sõber, Siim
    Sorice, Rossella
    Starr, John M
    Stott, David J
    Strachan, David P
    Strawbridge, Rona J
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Swertz, Morris A
    Taylor, Kent D
    Teumer, Alexander
    Tobin, Martin D
    Tomaszewski, Maciej
    Toniolo, Daniela
    Traglia, Michela
    Trompet, Stella
    Tuomilehto, Jaakko
    Tzourio, Christophe
    Uitterlinden, André G
    Vaez, Ahmad
    van der Most, Peter J
    van Duijn, Cornelia M
    Vergnaud, Anne-Claire
    Verwoert, Germaine C
    Vitart, Veronique
    Völker, Uwe
    Vollenweider, Peter
    Vuckovic, Dragana
    Watkins, Hugh
    Wild, Sarah H
    Willemsen, Gonneke
    Wilson, James F
    Wright, Alan F
    Yao, Jie
    Zemunik, Tatijana
    Zhang, Weihua
    Attia, John R
    Butterworth, Adam S
    Chasman, Daniel I
    Conen, David
    Cucca, Francesco
    Danesh, John
    Hayward, Caroline
    Howson, Joanna M M
    Laakso, Markku
    Lakatta, Edward G
    Langenberg, Claudia
    Melander, Olle
    Mook-Kanamori, Dennis O
    Palmer, Colin N A
    Risch, Lorenz
    Scott, Robert A
    Scott, Rodney J
    Sever, Peter
    Spector, Tim D
    van der Harst, Pim
    Wareham, Nicholas J
    Zeggini, Eleftheria
    Levy, Daniel
    Munroe, Patricia B
    Newton-Cheh, Christopher
    Brown, Morris J
    Metspalu, Andres
    Hung, Adriana M
    O'Donnell, Christopher J
    Edwards, Todd L
    Psaty, Bruce M
    Tzoulaki, Ioanna
    Barnes, Michael R
    Wain, Louise V
    Elliott, Paul
    Caulfield, Mark J
    Genetic analysis of over 1 million people identifies 535 new loci associated with blood pressure traits.2018Inngår i: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 50, nr 10, s. 1412-1425Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    High blood pressure is a highly heritable and modifiable risk factor for cardiovascular disease. We report the largest genetic association study of blood pressure traits (systolic, diastolic and pulse pressure) to date in over 1 million people of European ancestry. We identify 535 novel blood pressure loci that not only offer new biological insights into blood pressure regulation but also highlight shared genetic architecture between blood pressure and lifestyle exposures. Our findings identify new biological pathways for blood pressure regulation with potential for improved cardiovascular disease prevention in the future.

  • 75. Fall, Katja
    et al.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Bra prognosstudier kan ge bättre kliniska beslut2013Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 110, nr 6, s. 279-283Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [sv]

    Syftet med prognosstudier är primärt att skatta risken för ett utfall bland patienter på grupp- eller individnivå. För att kunna göra individuella riskbedömningar krävs prognosmodeller som baseras på risk- eller pro­gnosfaktorer.

    Modellens användbarhet är beroende av dess validitet och förmåga att korrekt skilja ut personer som i framtiden kommer att få ett ogynnsamt utfall från personer som inte kommer att få det.

    En kliniskt relevant risk- eller prognosfaktor (eller riskekvation som kombinerar flera sådana faktorer) kan kännas igen på att den när den används förändrar predicerad risk i hög grad och åt rätt håll, hos personer med en relevant absolut risk, vilket gör att den påverkar kliniskt beslutsfattande.

  • 76.
    Fall, Tove
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Mandic-Havelka, Aleksandra
    Karolinska Univ Hosp, Karolinska Inst & Clin Chem, Dept Mol Med & Surg.
    Helmersson, Johanna
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Sundstrom, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Reference Intervals for Fecal Calprotectin in Adults Using Two Different Extraction Methods in the Uppsala-SCAPIS Cohort.2017Inngår i: Clinical Laboratory, ISSN 1433-6510, Vol. 63, nr 9, s. 1493-1496Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Fecal calprotectin measurement is generally recommended to exclude inflammatory bowel disease (IBD) in patients with suspected IBD. A problem with the fecal calprotectin assays so far has been the rather long test-turnaround times. Recently a particle enhanced turbidimetric immunoassay (PETIA) for fecal calprotectin with assay times of approximately 10 minutes has been introduced on the European market. The aim of this study was to define reference intervals for adults with this new fecal calprotectin PETIA using two different extraction methods.

    Methods: Samples were collected from 382 healthy individuals from the Swedish CArdioPulmonary bioImage Study (SCAPIS) Uppsala cohort in the age range 50 - 65 years. 202 samples were processed with CALEX® Cap extraction device (BÜHLMANN, Schönenbuch, Switzerland) and 180 samples were extracted using weighed samples. The extracted samples were analyzed on a Mindray BS-380 using the fCal Turbo PETIA reagent (BÜHLMANN).

    Results: The calculated reference values for the Calex device were < 199 µg/g for the whole cohort, < 184 µg/g for females, and < 215 µg/g for males, while the corresponding values for weighed samples were < 153 µg/g for the whole cohort, < 141 µg/g for females, and < 215 µg/g for males. There were no significant statistical differences for calprotectin levels in males and females.

    Conclusions: The CALEX device yielded slightly higher calprotectin values. As there were no significant gender differences, the study indicates gender independent reference intervals of < 199 µg/g feces for the CALEX device and < 153 µg/g feces for weighed samples in patients in the 50 - 65 year age range.

  • 77. Fall, Tove
    et al.
    Shiue, Ivy
    af Geijerstam, Per Bergea
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Melhus, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk farmakogenomik och osteoporos.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Relations of circulating vitamin D concentrations with left ventricular geometry and function2012Inngår i: European Journal of Heart Failure, ISSN 1388-9842, E-ISSN 1879-0844, Vol. 14, nr 9, s. 985-991Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Vitamin D deficiency has been associated with risk of overt cardiovascular disease (CVD), but associations with subclinical disease are not well characterized. Hence, we examined associations of circulating vitamin D concentrations and left ventricular (LV) geometry and function by echocardiography at baseline and after 5 years in a community-based study. In the PIVUS study, we measured serum 25-dihydroxyvitamin-D (25-OH D) at age 70 and performed echocardiography including LV mass, wall thickness, end-diastolic diameter, end-systolic diameter (LVESD), left atrial diameter, fractional shortening, ejection fraction, isovolumic relaxation time, and E/A ratio at both age 70 and 75. We included 870 participants (52 women) without prior myocardial infarctions, heart failure, or prevalent valvular disease. After adjusting for potential confounders, 25-OH D at baseline was found to be significantly associated with LVESD, fractional shortening, and ejection fraction (, 0.42 mm, P 0.03; , 0.70, P 0.03; and , 0.91 P 0.01, respectively), per 1 SD increase in 25-OH D (SD 20 nmol/L) at baseline. In longitudinal analyses, vitamin D levels at baseline were not significantly associated with change in LV geometry and function after 5 years. In our community-based study among the elderly, we found higher circulating vitamin D concentrations to be associated cross-sectionally with better LV systolic function and smaller LVESD at baseline. The association persisted after adjusting for several potential confounders, including cardiovascular risk factors and calcium, phosphate, and parathyroid hormone levels. Randomized clinical trials are needed to establish firmly or refute a causal relationship between vitamin D levels and changes in LV geometry and function.

  • 78.
    Faxen, J.
    et al.
    Karolinska Inst, Dept Cardiol, Karolinska Univ Hosp, Stockholm, Sweden..
    Jernberg, T.
    Karolinska Inst, Dept Cardiol, Karolinska Univ Hosp, Stockholm, Sweden..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Lindahl, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Szummer, K.
    Karolinska Inst, Dept Cardiol, Karolinska Univ Hosp, Stockholm, Sweden..
    A risk score for predicting cardiac arrest requiring defibrillation or cardiopulmonary resuscitation for patients admitted with suspected non-ST-elevation acute coronary syndromes2015Inngår i: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 36, nr Suppl. 1, s. 406-406Artikkel i tidsskrift (Annet vitenskapelig)
  • 79. Faxen, J.
    et al.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Lindhagen, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Lindahl, Bertil
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Jernberg, T.
    Szummer, K.
    Predictors of in-hospital ventricular arrhythmias in patients admitted with suspected non-ST-elevation acute coronary syndrome: data from the SWEDEHEART registry2014Inngår i: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 35, s. 824-825Artikkel i tidsskrift (Fagfellevurdert)
  • 80. Faxén, Jonas
    et al.
    Hall, Marlous
    Gale, Chris P
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Lindahl, Bertil
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Jernberg, Tomas
    Szummer, Karolina
    A user-friendly risk-score for predicting in-hospital cardiac arrest among patients admitted with suspected non ST-elevation acute coronary syndrome - The SAFER-score2017Inngår i: Resuscitation, ISSN 0300-9572, E-ISSN 1873-1570, Vol. 121, s. 41-48Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    AIM: To develop a simple risk-score model for predicting in-hospital cardiac arrest (CA) among patients hospitalized with suspected non-ST elevation acute coronary syndrome (NSTE-ACS).

    METHODS: Using the Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies (SWEDEHEART), we identified patients (n=242 303) admitted with suspected NSTE-ACS between 2008 and 2014. Logistic regression was used to assess the association between 26 candidate variables and in-hospital CA. A risk-score model was developed and validated using a temporal cohort (n=126 073) comprising patients from SWEDEHEART between 2005 and 2007 and an external cohort (n=276 109) comprising patients from the Myocardial Ischaemia National Audit Project (MINAP) between 2008 and 2013.

    RESULTS: The incidence of in-hospital CA for NSTE-ACS and non-ACS was lower in the SWEDEHEART-derivation cohort than in MINAP (1.3% and 0.5% vs. 2.3% and 2.3%). A seven point, five variable risk score (age ≥60 years (1 point), ST-T abnormalities (2 points), Killip Class >1 (1 point), heart rate <50 or ≥100bpm (1 point), and systolic blood pressure <100mmHg (2 points) was developed. Model discrimination was good in the derivation cohort (c-statistic 0.72) and temporal validation cohort (c-statistic 0.74), and calibration was reasonable with a tendency towards overestimation of risk with a higher sum of score points. External validation showed moderate discrimination (c-statistic 0.65) and calibration showed a general underestimation of predicted risk.

    CONCLUSIONS: A simple points score containing five variables readily available on admission predicts in-hospital CA for patients with suspected NSTE-ACS.

  • 81.
    Figarska, Sylwia M.
    et al.
    Stanford Univ, Stanford Cardiovasc Inst, Stanford, CA 94305 USA;Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, 300 Pasteur Dr, Stanford, CA 94305 USA.
    Gustafsson, Stefan
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Ärnlöv, Johan
    Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Family Med & Primary Care, Huddinge, Sweden;Dalarna Univ, Sch Hlth & Social Sci, Falun, Sweden.
    Mälarstig, Anders
    Pfizer Worldwide Res & Dev, Stockholm, Sweden;Karolinska Inst, Dept Med Solna, Cardiovasc Med Unit, Stockholm, Sweden.
    Elmstahl, Sölve
    Lund Univ, Malmo Univ Hosp, Dept Clin Sci, Div Geriatr Med, Lund, Sweden.
    Fall, Tove
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Stanford Univ, Stanford Cardiovasc Inst, Stanford, CA 94305 USA;Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, 300 Pasteur Dr, Stanford, CA 94305 USA.
    Associations of Circulating Protein Levels With Lipid Fractions in the General Population2018Inngår i: Arteriosclerosis, Thrombosis and Vascular Biology, ISSN 1079-5642, E-ISSN 1524-4636, Vol. 38, nr 10, s. 2505-2518Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: Revealing patterns of associations between circulating protein and lipid levels could improve biological understanding of cardiovascular disease (CVD). In this study, we investigated the associations between proteins related to CVD and triglyceride (TG), total cholesterol, LDL (low-density lipoprotein), and HDL (high-density lipoprotein) cholesterol levels in individuals from the general population.

    Approach and Results: We measured plasma protein levels using the Olink ProSeek CVD I or II+III arrays and analyzed 57 proteins available in 3 population-based cohorts: EpiHealth (n=2029; 52% women; median age, 61 years), PIVUS (Prospective Study of the Vasculature in Uppsala Seniors; n=790; 51% women; all aged 70 years), and ULSAM (Uppsala Longitudinal Study of Adult Men; n=551; all men aged 77 years). A discovery analysis was performed in EpiHealth in a regression framework (adjusted for sex, age, body mass index, smoking, glucose levels, systolic blood pressure, blood pressure medication, diabetes mellitus medication, and CVD history), and associations with false discovery rate <0.05 were further tested in PIVUS and ULSAM, where a P value of 0.05 was considered a successful replication (validation false discovery rate of 0.1%). We used summary statistics from a genome-wide association study on each protein biomarker (meta-analysis of EpiHealth, PIVUS, ULSAM, and IMPROVE [Carotid Intima-Media Thickness and IMT-Progression as Predictors of Vascular Events in a High-Risk European Population]) and publicly available data from Global Lipids Genetics Consortium to perform Mendelian randomization analyses to address possible causality of protein levels. Of 57 tested proteins, 42 demonstrated an association with at least 1 lipid fraction; 35 were associated with TG, 15 with total cholesterol, 9 with LDL cholesterol, and 24 with HDL cholesterol. Among these associations, we found KIM-1 (kidney injury molecule-1), TNFR (TNF [tumor necrosis factor] receptor) 1 and 2, TRAIL-R2 (TRAIL [TNF-related apoptosis-inducing ligand] receptor 2), and RETN (resistin) to be associated with all 4 lipid fractions. Further, 15 proteins were related to both TG and HDL cholesterol in a consistent and biologically expected manner, that is, higher TG and lower HDL cholesterol or vice versa. Another common pattern of associations was concomitantly higher TG, total cholesterol, and LDL cholesterol, which is associated with higher CVD risk. We did not find evidence of causal links for protein levels.

    Conclusions: Our comprehensive analysis of plasma proteins and lipid fractions of 3370 individuals from the general population provides new information about lipid metabolism.

  • 82.
    Ganna, Andrea
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Magnusson, Patrik K. E.
    Pedersen, Nancy L.
    de Faire, Ulf
    Reilly, Marie
    Arnloe, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Hamsten, Anders
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Multilocus Genetic Risk Scores for Coronary Heart Disease Prediction2013Inngår i: Arteriosclerosis, Thrombosis and Vascular Biology, ISSN 1079-5642, E-ISSN 1524-4636, Vol. 33, nr 9, s. 2267-2272Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective-Current guidelines do not support the use of genetic profiles in risk assessment of coronary heart disease (CHD). However, new single nucleotide polymorphisms associated with CHD and intermediate cardiovascular traits have recently been discovered. We aimed to compare several multilocus genetic risk score (MGRS) in terms of association with CHD and to evaluate clinical use. Approach and Results-We investigated 6 Swedish prospective cohort studies with 10 612 participants free of CHD at baseline. We developed 1 overall MGRS based on 395 single nucleotide polymorphisms reported as being associated with cardiovascular traits, 1 CHD-specific MGRS, including 46 single nucleotide polymorphisms, and 6 trait-specific MGRS for each established CHD risk factors. Both the overall and the CHD-specific MGRS were significantly associated with CHD risk (781 incident events; hazard ratios for fourth versus first quartile, 1.54 and 1.52; P<0.001) and improved risk classification beyond established risk factors (net reclassification improvement, 4.2% and 4.9%; P=0.006 and 0.017). Discrimination improvement was modest (C-index improvement, 0.004). A polygene MGRS performed worse than the CHD-specific MGRS. We estimate that 1 additional CHD event for every 318 people screened at intermediate risk could be saved by measuring the CHD-specific genetic score in addition to the established risk factors. Conclusions-Our results indicate that genetic information could be of some clinical value for prediction of CHD, although further studies are needed to address aspects, such as feasibility, ethics, and cost efficiency of genetic profiling in the primary prevention setting.

  • 83.
    Ganna, Andrea
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Salihovic, Samira
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Broeckling, Corey D
    Proteomics and Metabolomics Facility, Colorado State University, Fort Collins, Colorado, United States of America.
    Hedman, Åsa K
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Magnusson, Patrik K E
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Pedersen, Nancy L
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Siegbahn, Agneta
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Koagulation och inflammationsvetenskap.
    Zilmer, Mihkel
    Department of Biochemistry, Centre of Excellence for Translational Medicine, University of Tartu, Tartu, Estonia.
    Prenni, Jessica
    Proteomics and Metabolomics Facility, Colorado State University, Fort Collins, Colorado, United States of America.
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Fall, Tove
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Large-scale Metabolomic Profiling Identifies Novel Biomarkers for Incident Coronary Heart Disease2014Inngår i: PLOS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 10, nr 12, s. e1004801-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Analyses of circulating metabolites in large prospective epidemiological studies could lead to improved prediction and better biological understanding of coronary heart disease (CHD). We performed a mass spectrometry-based non-targeted metabolomics study for association with incident CHD events in 1,028 individuals (131 events; 10 y. median follow-up) with validation in 1,670 individuals (282 events; 3.9 y. median follow-up). Four metabolites were replicated and independent of main cardiovascular risk factors [lysophosphatidylcholine 18∶1 (hazard ratio [HR] per standard deviation [SD] increment = 0.77, P-value<0.001), lysophosphatidylcholine 18∶2 (HR = 0.81, P-value<0.001), monoglyceride 18∶2 (MG 18∶2; HR = 1.18, P-value = 0.011) and sphingomyelin 28∶1 (HR = 0.85, P-value = 0.015)]. Together they contributed to moderate improvements in discrimination and re-classification in addition to traditional risk factors (C-statistic: 0.76 vs. 0.75; NRI: 9.2%). MG 18∶2 was associated with CHD independently of triglycerides. Lysophosphatidylcholines were negatively associated with body mass index, C-reactive protein and with less evidence of subclinical cardiovascular disease in additional 970 participants; a reverse pattern was observed for MG 18∶2. MG 18∶2 showed an enrichment (P-value = 0.002) of significant associations with CHD-associated SNPs (P-value = 1.2×10-7 for association with rs964184 in the ZNF259/APOA5 region) and a weak, but positive causal effect (odds ratio = 1.05 per SD increment in MG 18∶2, P-value = 0.05) on CHD, as suggested by Mendelian randomization analysis. In conclusion, we identified four lipid-related metabolites with evidence for clinical utility, as well as a causal role in CHD development.

  • 84. Garcia, Julianne
    et al.
    Dunford, Elizabeth K
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Neal, Bruce C
    Changes in the sodium content of leading Australian fast-food products between 2009 and 20122014Inngår i: Medical Journal of Australia, ISSN 0025-729X, E-ISSN 1326-5377, Vol. 200, nr 6, s. 340-344Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To define the changes in sodium levels of Australian fast foods between 2009 and 2012 overall, in major food subcategories and by company.

    DESIGN: A comparison of mean sodium content was made across 4 years using t tests and mixed models.

    SETTING: Nutrient content data for fast-food menu items collected from company websites of six large Australian fast-food chains.

    MAIN OUTCOME MEASURES: Mean sodium values in mg/100 g and mg/serve.

    RESULTS: There were between 302 and 381 products identified each year. Overall, the mean sodium content of fast-food products decreased between 2009 and 2012 by 43 mg/100 g (95% CI, - 66 to - 20 mg/100 g), from 514 mg/100 g in 2009 to 471 mg/100 g in 2012. Mean sodium content per serving was not significantly different at 654 mg in 2009 and 605 mg in 2012 (- 49 mg; 95% CI, - 108 to + 10 mg), reflecting wide variation in the serving sizes of items offered each year. There was a small decline in sodium content over the 4 years across most food categories and food companies.

    CONCLUSIONS: The observed reduction in the sodium content of fast foods during the 4-year study period is encouraging. However, the reductions are small, and fast-food companies should be encouraged to make further and larger reductions since many products still contain high levels of sodium.

  • 85. Grundvold, I.
    et al.
    Bodegard, J.
    Nilsson, P. M.
    Svennblad, Bodil
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Johansson, G.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Ostgren, C. J.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Body mass index and changes in weight are associated with risk of atrial fibrillation and cardiovascular mortality: a longitudinal cohort study of 7,169 patients with newly diagnosed type 2 diabetes2014Inngår i: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 35, s. 539-539Artikkel i tidsskrift (Fagfellevurdert)
  • 86. Grundvold, Irene
    et al.
    Bodegard, Johan
    Nilsson, Peter M.
    Svennblad, Bodil
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Johansson, Gunnar
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    Ostgren, Carl Johan
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Body weight and risk of atrial fibrillation in 7,169 patients with newly diagnosed type 2 diabetes; an observational study2015Inngår i: Cardiovascular Diabetology, ISSN 1475-2840, E-ISSN 1475-2840, Vol. 14, s. 5-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Obesity, type 2 diabetes and atrial fibrillation (AF) are closely associated, but the underlying mechanisms are not fully understood. We aimed to explore associations between body mass index (BMI) or weight change with risk of AF in patients with type 2 diabetes. Methods: A total of 7,169 participations with newly diagnosed type 2 diabetes were stratified according to baseline BMI, and after a second BMI measurement within 18 months, further grouped according to relative weight change as "weight gain" (> 1 BMI unit), " stable weight" (+/- 1 BMI unit) and " weight loss" (< 1 BMI unit). The mean follow-up period was 4.6 years, and the risk of AF was estimated using adjusted Cox regression models. Results: Average age at diabetes diagnosis was 60 years and the patients were slightly obese (mean BMI 30.2 kg/m(2)). During follow-up, 287 patients developed incident AF, and those with overweight or obesity at baseline had 1.9 fold and 2.9-fold higher risk of AF, respectively, than those with normal BMI. The 14% of the patients with subsequent weight gain had 1.5-fold risk of AF compared with those with stable weight or weight loss. Conclusions: In patients with newly diagnosed type 2 diabetes, baseline overweight and obesity, as well as modest weight increase during the first 18 months after diagnosis, were associated with a substantially increased risk of incident AF. Patients with type 2 diabetes may benefit from efforts to prevent weight gain in order to reduce the risk of incident AF.

  • 87.
    Hagström, Emil
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi.
    Hellman, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi.
    Larsson, Tobias E.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Berglund, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Melhus, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Held, Claes
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Plasma parathyroid hormone and the risk of cardiovascular mortality in the community2009Inngår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 119, nr 21, s. 2765-2771Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Diseases with elevated levels of parathyroid hormone (PTH) such as primary and secondary hyperparathyroidism are associated with increased incidence of cardiovascular disease and death. However, data on the prospective association between circulating PTH levels and cardiovascular mortality in the community are lacking. METHODS AND RESULTS: The Uppsala Longitudinal Study of Adult Men (ULSAM), a community-based cohort of elderly men (mean age, 71 years; n=958), was used to investigate the association between plasma PTH and cardiovascular mortality. During follow-up (median, 9.7 years), 117 participants died of cardiovascular causes. In Cox proportional-hazards models adjusted for established cardiovascular risk factors (age, systolic blood pressure, diabetes, smoking, body mass index, total cholesterol, high-density lipoprotein cholesterol, antihypertensive treatment, lipid-lowering treatment, and history of cardiovascular disease), higher plasma PTH was associated with higher risk for cardiovascular mortality (hazard ratio for 1-SD increase in PTH, 1.38; 95% confidence interval, 1.18 to 1.60; P<0.001). This association remained essentially unaltered in participants without previous cardiovascular disease and in participants with normal PTH (<6.8 pmol/L) with no other signs of a disturbed mineral metabolism (normal serum calcium, 2.2 to 2.6 mmol/L; normal glomerular filtration rate, >50 mL . min(-1) . 1.73 m(-2) and without vitamin D deficiency, plasma 25-OH vitamin D >37.5 nmol/L). Interestingly, elevated plasma PTH (>5.27 pmol/L) accounted for 20% (95% confidence interval, 10 to 26) of the population-attributable risk proportion for cardiovascular mortality. CONCLUSIONS: Plasma PTH levels predict cardiovascular mortality in the community, even in individuals with PTH within the normal range. Further studies are warranted to evaluate the clinical implications of measuring PTH in cardiovascular risk prediction and to elucidate whether PTH is a modifiable risk factor.

  • 88.
    Hagström, Emil
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Melhus, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk farmakogenomik och osteoporos.
    Hansen, Tomas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Ahlström, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Johansson, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Arnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Plasma-Parathyroid Hormone Is Associated With Subclinical and Clinical Atherosclerotic Disease in 2 Community-Based Cohorts2014Inngår i: Arteriosclerosis, Thrombosis and Vascular Biology, ISSN 1079-5642, E-ISSN 1524-4636, Vol. 34, nr 7, s. 1567-73Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: Cardiovascular risk factors have different impact on different arterial territories. Diseases with elevated circulating parathyroid hormone (PTH) such as primary hyperparathyroidism and chronic renal failure have been shown to be associated with an increased risk of cardiovascular disease, predominantly heart or cerebrovascular diseases. However, data on the associations between circulating PTH and peripheral atherosclerosis are limited.

    APPROACH AND RESULTS: Two prospective, community-based studies were used. In 306 men and women, who were 70 years old, from the Prospective investigation of the vasculature in Uppsala seniors (PIVUS) study, cross-sectional relations between PTH and atherosclerotic burden assessed by whole-body magnetic resonance angiography were investigated. In 998 men, who were 71 years old, from the Uppsala longitudinal study of adult men (ULSAM) study, the association between PTH concentration and risk of subsequent nonfatal atherosclerotic disease (excluding coronary or cerebrovascular disease) was investigated. Adjusting for established vascular risk factors, PTH was associated with burden of atherosclerosis (increase in total atherosclerotic score per SD PTH increase: 0.04, 0.003-0.08; P=0.03) in the PIVUS study. During follow-up in the ULSAM study (median 16.7 years), 89 men were diagnosed with nonfatal atherosclerotic disease. In Cox-regression analyses adjusting for established vascular risk factors and mineral metabolism, higher PTH was associated with an increased risk of nonfatal atherosclerotic disease (hazard ratio for 1 SD increase of PTH: 1.55, 1.33-1.88; P<0.0001). Results were similar when including fatal atherosclerotic disease in the outcome.

    CONCLUSIONS: In 2 independent community-based cohorts, PTH was associated to the degree of atherosclerosis and risk of clinically overt atherosclerotic disease, respectively. Our data confirm and extend previous studies supporting a role for PTH in the development of atherosclerotic disease.

  • 89.
    Hansson, Jonas
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Hulthe, Johannes
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Relations of serum MMP-9 and TIMP-1 levels to left ventricular measures and cardiovascular risk factors: a population-based study2009Inngår i: European Journal of Cardiovascular Prevention & Rehabilitation, ISSN 1741-8267, E-ISSN 1741-8275, Vol. 16, nr 3, s. 297-303Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Extracellular matrix remodeling is a hallmark of pathological left ventricular (LV) hypertrophy and heart failure. This process is tightly controlled by the degrading matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). We hypothesized that circulating MMP-9 and TIMP-1 levels are altered already in persons with the signs of LV remodeling that forego clinical heart failure. DESIGN: Cross-sectional study in the Prospective Investigation of the Vasculature in Uppsala Seniors , a community-based cohort of 891 70-year-old men and women free from valvular disease, heart failure, and myocardial infarction. METHODS: We examined relations of serum MMP-9 and TIMP-1 to echocardiographic LV geometry and function. All models were adjusted for sex, height, intra-arterial systolic and diastolic blood pressures, antihypertensive medication use, and serum freezer time. RESULTS: Serum TIMP-1 was positively related to LV mass and wall thickness (r=0.15, P<0.0001 and r=0.16, P<0.0001, respectively), with a 32 g higher LV mass and 2.2 mm thicker walls in the fourth compared with the first quartile of serum TIMP-1. Serum TIMP-1 was also inversely related to LV ejection fraction (r=-0.10, P=0.009), but not to LV dimension or diastolic function indices. Serum MMP-9 was only weakly related to LV wall thickness and isovolumic relaxation time (r=0.08, P=0.04 and r=-0.08, P=0.04). CONCLUSION: In this large population-based sample, serum TIMP-1 levels were related to LV mass, wall thickness, and inversely to systolic function. This may imply that extracellular matrix remodeling is involved already in the earliest stages of the process leading to heart failure.

  • 90. Hasvold, L. P.
    et al.
    Bodegard, J.
    Thuresson, M.
    Stålhammar, Jan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    Hammar, N.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Russell, D.
    Kjeldsen, S. E.
    Diabetes and CVD risk during angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker treatment in hypertension: a study of 15 990 patients2014Inngår i: Journal of Human Hypertension, ISSN 0950-9240, E-ISSN 1476-5527, Vol. 28, nr 11, s. 663-669Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Differences in clinical effectiveness between angiotensin-converting enzyme inhibitors (ACEis) and angiotensin receptor blockers (ARBs) in the primary treatment of hypertension are unknown. The aim of this retrospective cohort study was to assess the prevention of type 2 diabetes and cardiovascular disease (CVD) in patients treated with ARBs or ACEis. Patients initiated on enalapril or candesartan treatment in 71 Swedish primary care centers between 1999 and 2007 were included. Medical records data were extracted and linked with nationwide hospital discharge and cause of death registers. The 11 725 patients initiated on enalapril and 4265 on candesartan had similar baseline characteristics. During a mean follow-up of 1.84 years, 36 482 patient-years, the risk of new diabetes onset was lower in the candesartan group (hazard ratio (HR) 0.81, 95% confidence interval (CI) 0.69-0.96, P = 0.01) compared with the enalapril group. No difference between the groups was observed in CVD risk (HR 0.99, 95% CI 0.87-1.13, P = 0.86). More patients discontinued treatment in the enalapril group (38.1%) vs the candesartan group (27.2%). In a clinical setting, patients initiated on candesartan treatment had a lower risk of new-onset type 2 diabetes and lower rates of drug discontinuation compared with patients initiated on enalapril. No differences in CVD risk were observed.

  • 91.
    Hasvold, Pal
    et al.
    AstraZeneca, S-15185 Sodertalje, Sweden.;Univ Oslo, Fac Med, N-0424 Oslo, Norway..
    Thuresson, Marcus
    Statisticon AB, S-75322 Uppsala, Sweden..
    Sundstrom, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Hammar, Niklas
    Karolinska Inst, Inst Environm Med, S-17177 Stockholm, Sweden.;AZ R&D, Med Evidence & Observat Res, Molndal, Sweden..
    Kjeldsen, Sverre E.
    Univ Oslo, Fac Med, N-0424 Oslo, Norway.;Oslo Univ Hosp, Dept Cardiol, Oslo, Norway..
    Johansson, Gunnar
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Allmänmedicin och preventivmedicin.
    Holme, Ingar
    Norwegian Sch Sport Sci, Dept Sports Med, POB 4014, N-0806 Oslo, Norway..
    Bodegard, Johan
    AstraZeneca, S-15185 Sodertalje, Sweden..
    Association Between Paradoxical HDL Cholesterol Decrease and Risk of Major Adverse Cardiovascular Events in Patients Initiated on Statin Treatment in a Primary Care Setting2016Inngår i: Clinical drug investigation, ISSN 1173-2563, E-ISSN 1179-1918, Vol. 36, nr 3, s. 225-233Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and Objectives Statin-induced changes in high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) are unrelated. Many patients initiated on statins experience a paradoxical decrease in HDL-C. The aim of this study was to evaluate the association between a decrease in HDL-C and risk of major adverse cardiovascular events (MACE). Methods Data from 15,357 primary care patients initiated on statins during 2004-2009 were linked with data from mandatory national hospital, drug-dispensing, and cause-of-death registers, and were grouped according to HDL-C change: decreased >= 0.1 mmol/L, unchanged +/- 0.1 or >= 0.1 mmol/L increased. To evaluate the association between decrease in HDL-C and risk of MACE, a sample of propensity score-matched patients from the decreased and unchanged groups was created, using the latter group as reference. MACE was defined as myocardial infarction, unstable angina pectoris, ischaemic stroke, or cardiovascular mortality. Cox proportional hazards models were used to estimate relative risks. Results HDL-C decreased in 20 %, was unchanged in 58%, and increased in 22 % of patients initiated on statin treatment (96 % treated with simvastatin). The propensity score-matched sample comprised 5950 patients with mean baseline HDL-C and LDL-C of 1.69 and 4.53 mmol/L, respectively. HDL-C decrease was associated with 56 % higher MACE risk (hazard ratio 1.56; 95 % confidence interval 1.12-2.16; p < 0.01) compared with the unchanged HDL-C group. Conclusions Paradoxical statin-induced reduction in HDL-C was relatively common and was associated with increased risk of MACE.

  • 92.
    Hedberg, Jakob
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Gastrointestinalkirurgi.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Sundbom, Magnus
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Gastrointestinalkirurgi.
    Duodenal switch versus Roux-en-Y gastric bypass for morbid obesity: systematic review and meta-analysis of weight results, diabetes resolution and early complications in single-centre comparisons2014Inngår i: Obesity Reviews, ISSN 1467-7881, E-ISSN 1467-789X, Vol. 15, nr 7, s. 555-563Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Long-term weight loss after Roux-en-Y gastric bypass (RYGB) in super-obese patients has not been ideal. Biliopancreatic diversion with duodenal switch (DS) is argued to be better; however, additional side effects are feared. The aim of the present study was to determine differences in results after DS and RYGB in publications from single-centre comparisons. A systematic review of studies containing DS and RYGB performed at the same centre was performed. Outcome data were weight results, resolution of comorbid conditions, perioperative results and complications. Main outcome was difference in weight loss after DS and RYGB. Secondary outcomes were difference in resolution of comorbidities, perioperative results and complications. The final analysis included 16 studies with in total 874 DS and 1,149 RYGB operations. When comparing weight results at the longest follow-up of each study, DS yielded 6.2 (95% confidence interval 5.0-7.5) body mass index units additional weight loss compared with RYGB, P < 0.001. Operative time and length of stay were significantly longer after DS, as well as the risk for post-operative leaks, P < 0.05. DS is more effective than RYGB as a weight-reducing procedure. However, this comes at the price of more early complications and might also yield slightly higher perioperative mortality.

  • 93.
    Hedberg, Jakob
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Gastrointestinalkirurgi.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Thuresson, M.
    Aarskog, P.
    Oldgren, Jonas
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi.
    Bodegard, J.
    Low-dose acetylsalicylic acid and gastrointestinal ulcers or bleeding - a cohort study of the effects of proton pump inhibitor use patterns2013Inngår i: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 274, nr 4, s. 371-380Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective The aim of this study was to investigate the associations between proton pump inhibitor (PPI) usage patterns and risk of severe gastrointestinal events in patients treated with low-dose acetylsalicylic acid (LDA). Design and setting A nationwide cohort study in Sweden. Patients All Swedish residents 40years of age, without cancer and receiving LDA treatment (80% adherence for 365days between 2005 and 2009) were identified in the Swedish Prescription Register. Continuous PPI use was defined as >60 of 90days covered by daily PPI doses and further divided into high (80%) or moderate (<80) adherence. All other PPI use was defined as intermittent use. Main outcome measures The risk of a combined end-point of gastrointestinal ulcer or bleeding was analysed using Cox proportional hazard models. We also investigated risk of >45days of LDA treatment interruption. Results During a median follow-up of 2.5years, 7880 of 648807 (1.2%) LDA-treated patients experienced gastrointestinal events. In multivariable-adjusted models, both intermittent-PPI and no-PPI use were associated with increased risk of gastrointestinal ulcers or bleeding compared with continuous PPI use with a high level of adherence [hazard ratio (HR) 1.83 (95% CI 1.66-2.02) and 1.14 (95% CI 1.05-1.23), respectively]. Amongst continuous PPI users, moderate adherence also increased the risk of gastrointestinal ulcers or bleeding [HR 1.22 (95% CI 1.07-1.40)]. The risk of LDA treatment interruption was higher with intermittent PPI use [HR 1.16 (95% CI 1.14-1.19)] than continuous PPI use with high adherence. Conclusions In this large cohort of LDA users, intermittent PPI use was associated with higher risk of gastrointestinal ulcers or bleeding and interrupted LDA treatment, compared with continuous PPI use.

  • 94.
    Hedman, Åsa K.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Karolinska Inst, Dept Med Solna, Cardiovasc Med Unit, Stockholm, Sweden..
    Mendelson, Michael M.
    Framingham Heart Dis Epidemiol Study, Framingham, MA USA.;Boston Univ, Boston, MA 02215 USA.;Boston Childrens Hosp, Dept Cardiol, Boston, MA USA.;NHLBI, Populat Sci Branch, NIH, Bldg 10, Bethesda, MD 20892 USA..
    Marioni, Riccardo E.
    Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh EH8 9YL, Midlothian, Scotland.;Univ Edinburgh, Inst Genet & Mol Med, Ctr Genom & Expt Med, Med Genet Sect, Edinburgh EH8 9YL, Midlothian, Scotland.;Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia..
    Gustafsson, Stefan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Joehanes, Roby
    Framingham Heart Dis Epidemiol Study, Framingham, MA USA.;NHLBI, Populat Sci Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.;Harvard Med Sch, Hebrew Senior Life, Boston, MA USA..
    Irvin, Marguerite R.
    Univ Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA..
    Zhi, Degui
    Univ Alabama Birmingham, Dept Biostat, Sect Stat Genet, Birmingham, AL 35294 USA..
    Sandling, Johanna K.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär medicin. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Yao, Chen
    Framingham Heart Dis Epidemiol Study, Framingham, MA USA.;NHLBI, Populat Sci Branch, NIH, Bldg 10, Bethesda, MD 20892 USA..
    Liu, Chunyu
    Framingham Heart Dis Epidemiol Study, Framingham, MA USA.;Boston Univ, Dept Biosci, Boston, MA 02215 USA.;NHLBI, Populat Sci Branch, NIH, Bldg 10, Bethesda, MD 20892 USA..
    Liang, Liming
    Harvard Sch Publ Hlth, Dept Biostat, Boston, MA USA..
    Huan, Tianxiao
    Framingham Heart Dis Epidemiol Study, Framingham, MA USA.;NHLBI, Populat Sci Branch, NIH, Bldg 10, Bethesda, MD 20892 USA..
    McRae, Allan F.
    Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia.;Univ Queensland, Inst Mol Biosci, Brisbane, Qld, Australia..
    Demissie, Serkalem
    Framingham Heart Dis Epidemiol Study, Framingham, MA USA.;Boston Univ, Dept Biosci, Boston, MA 02215 USA..
    Shah, Sonia
    Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia.;Univ Queensland, Inst Mol Biosci, Brisbane, Qld, Australia..
    Starr, John M.
    Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh EH8 9YL, Midlothian, Scotland.;Univ Edinburgh, Alzheimer Scotland Dementia Res Ctr, Edinburgh EH8 9YL, Midlothian, Scotland..
    Cupples, L. Adrienne
    Framingham Heart Dis Epidemiol Study, Framingham, MA USA.;Boston Univ, Dept Biosci, Boston, MA 02215 USA..
    Deloukas, Panos
    Queen Mary Univ London, Barts & London Sch Med & Dent, William Harvey Res Inst, London, England.;King Abdulaziz Univ, Princess Al Jawhara Al Brahim Ctr Excellence Res, Jeddah, Saudi Arabia..
    Spector, Timothy D.
    Kings Coll London, Dept Twin Res & Genet Epidemiol, London WC2R 2LS, England..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Krauss, Ronald M.
    Childrens Hosp Oakland, Res Inst, Oakland, CA 94609 USA..
    Arnett, Donna K.
    Univ Kentucky, Coll Publ Hlth, Lexington, KY 40506 USA..
    Deary, Ian J.
    Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh EH8 9YL, Midlothian, Scotland.;Univ Edinburgh, Dept Psychol, Edinburgh EH8 9YL, Midlothian, Scotland..
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Levy, Daniel
    Framingham Heart Dis Epidemiol Study, Framingham, MA USA.;NHLBI, Populat Sci Branch, NIH, Bldg 10, Bethesda, MD 20892 USA..
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, 300 Pasteur Dr,Mail Code 5773, Stanford, CA 94305 USA..
    Epigenetic Patterns in Blood Associated With Lipid Traits Predict Incident Coronary Heart Disease Events and Are Enriched for Results From Genome-Wide Association Studies2017Inngår i: Circulation: Cardiovascular Genetics, ISSN 1942-325X, E-ISSN 1942-3268, Vol. 10, nr 1, artikkel-id UNSP e001487Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background- Genome-wide association studies have identified loci influencing circulating lipid concentrations in humans; further information on novel contributing genes, pathways, and biology may be gained through studies of epigenetic modifications. Methods and Results- To identify epigenetic changes associated with lipid concentrations, we assayed genome-wide DNA methylation at cytosine-guanine dinucleotides (CpGs) in whole blood from 2306 individuals from 2 population-based cohorts, with replication of findings in 2025 additional individuals. We identified 193 CpGs associated with lipid levels in the discovery stage (P < 1.08E-07) and replicated 33 (at Bonferroni-corrected P < 0.05), including 25 novel CpGs not previously associated with lipids. Genes at lipid-associated CpGs were enriched in lipid and amino acid metabolism processes. A differentially methylated locus associated with triglyceridesand high-density lipoprotein cholesterol (HDL- C; cg27243685; P= 8.1E-26 and 9.3E-19) was associated with cis-expression of a reverse cholesterol transporter (ABCG1; P= 7.2E-28) and incident cardiovascular disease events (hazard ratio per SD increment, 1.38; 95% confidence interval, 1.15-1.66; P= 0.0007). We found significant cis-methylation quantitative trait loci at 64% of the 193 CpGs with an enrichment of signals from genome-wide association studies of lipid levels (P-TC = 0.004, PHDL-C = 0.008 and P-triglycerides = 0.00003) and coronary heart disease ( P= 0.0007). For example, genome-wide significant variants associated with low-density lipoprotein cholesterol and coronary heart disease at APOB were cis-methylation quantitative trait loci for a low-density lipoprotein cholesterol-related differentially methylated locus. Conclusions-We report novel associations of DNA methylation with lipid levels, describe epigenetic mechanisms related to previous genome-wide association studies discoveries, and provide evidence implicating epigenetic regulation of reverse cholesterol transport in blood in relation to occurrence of cardiovascular disease events.

  • 95.
    Hedman, Åsa K.
    et al.
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi.
    Zilmer, Mihkel
    Univ Tartu, Inst Biomed & Translat Med, Dept Biochem, Ctr Excellence Genom & Translat Med, Tartu, Estonia..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, Stanford, CA 94305 USA..
    DNA methylation patterns associated with oxidative stress in an ageing population2016Inngår i: BMC Medical Genomics, ISSN 1755-8794, E-ISSN 1755-8794, Vol. 9, artikkel-id 72Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Oxidative stress has been related to type 2 diabetes (T2D) and cardiovascular disease (CVD), the leading global cause of death. Contributions of environmental factors such as oxidative stress on complex traits and disease may be partly mediated through changes in epigenetic marks (e.g. DNA methylation). Studies relating differential methylation with intermediate phenotypes and disease endpoints may be useful in identifying additional candidate genes and mechanisms involved in disease. Methods: To investigate the role of epigenetic variation in oxidative stress marker levels and subsequent development of CVD and T2D, we performed analyses of genome-wide DNA methylation in blood, ten markers of oxidative stress (total glutathione [TGSH], reduced glutathione [GSH], oxidised glutathione [GSSG], GSSG to GSH ratio, homocysteine [HCY], oxidised low-density lipoprotein (oxLDL), antibodies against oxLDL [OLAB], conjugated dienes [CD], baseline conjugated dienes [BCD]-LDL and total antioxidant capacity [TAOC]) and incident disease in up to 966 age-matched individuals. Results: In total, we found 66 cytosine-guanine (CpG) sites associated with one or more oxidative stress markers (false discovery rate [FDR] <0.05). These sites were enriched in regulatory regions of the genome. Genes annotated to CpG sites showed enrichment in annotation clusters relating to phospho-metabolism and proteins with pleckstrin domains. We investigated the contribution of oxidative stress-associated CpGs to development of cardiometabolic disease. Methylation variation at CpGs in the 3'-UTR of HIST1H4D (cg08170869; histone cluster 1, H4d) and in the body of DVL1 (cg03465880; dishevelled-1) were associated with incident T2D events during 10 years of follow-up (all permutation p-values < 0.01), indicating a role of epigenetic regulation in oxidative stress processes leading to development or progression of diabetes. Methylation QTL (meQTL) analysis showed significant associations with genetic sequence variants in cis at 28 (42%) of oxidative stress phenotype-associated sites (FDR < 0.05). Integrating cis-meQTLs with genotype-phenotype associations indicated that genetic effects on oxidative stress phenotype at one locus (cg07547695; BCL2L11) may be mediated through DNA methylation. Conclusions: In conclusion, we report novel associations of DNA methylation with oxidative stress, some of which also show evidence of a relation with T2D incidence.

  • 96.
    Helmersson-Karlqvist, Johanna
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Carlsson, Axel C
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Venge, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Ingelsson, Erik
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Urinary neutrophil gelatinase-associated lipocalin (NGAL) is associated with mortality in a community-based cohort of older Swedish men2013Inngår i: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 227, nr 2, s. 408-413Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE

    Neutrophil gelatinase-associated lipocalin (NGAL) indicates tubular kidney damage, neutrophil activation and possibly atherogenesis, however the prospective association between urinary NGAL (u-NGAL) and cardiovascular death in the community is not known.

    METHODS

    This study evaluates the association between urinary and serum NGAL and mortality in a Swedish population of 597 men aged 78 years. During the study (median follow-up 8.1 years) 261 men died, 90 of cardiovascular causes.

    RESULTS

    U-NGAL was associated with increased all-cause and cardiovascular mortality (HR 2.0 for quartile 4 vs. quartile 1, 95% CI 1.0-4.0, P < 0.05) in Cox regression models independently of cardiovascular risk factors, CRP and cystatin C estimated glomerular filtration rate (eGFRCysC) but not urinary Albumin (u-Alb). A combination of low eGFRCysC (≤60 mL/min), high u-Alb (≥3 mg/mmol Cr) and high u-NGAL (≥1.19 μg/mmol Cr) was associated with a 9-fold increased cardiovascular mortality (P < 0.001) and a 3-fold increased all-cause mortality (P < 0.001). Serum NGAL was associated with increased all-cause mortality risk independent of other cardiovascular risk factors (HR 1.4 for quartile 4 vs.1, 95% CI 1.0-1.9, P < 0.05) but not after adjustment with CRP, eGFRCysC or u-Alb.

    CONCLUSION

    This community study is the first to show that the tubular kidney biomarker u-NGAL associated with increased cardiovascular and all-cause mortality independent of cardiovascular risk factors and glomerular filtration. Additional research is needed to evaluate the utility of NGAL in clinical practice.

  • 97. Hemmingsson, Erik
    et al.
    Johansson, Kari
    Eriksson, Jonas
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Neovius, Martin
    Marcus, Claude
    Weight loss and dropout during a commercial weight-loss program including a very-low-calorie diet, a low-calorie diet, or restricted normal food: observational cohort study2012Inngår i: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 96, nr 5, s. 953-961Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The effectiveness of commercial weight-loss programs consisting of very-low-calorie diets (VLCDs) and low-calorie diets (LCDs) is unclear. Objective: The aim of the study was to quantify weight loss and dropout during a commercial weight-loss program in Sweden (Itrim; cost: $1300/(sic)1000; all participants paid their own fee). Design: This observational cohort study linked commercial weight-loss data with National Health Care Registers. Weight loss was induced with a 500-kcal liquid-formula VLCD [n = 3773; BMI (in kg/m(2)): 34 +/- 5 (mean +/- SD); 80% women; 45 +/- 12 y of age (mean +/- SD)], a 1200-1500-kcal formula and food-combination LCD (n = 4588; BMI: 30 +/- 4; 86% women; 50 +/- 11 y of age), and a 1500-1800-kcal/d restricted normal-food diet (n = 676; BMI: 29 +/- 5; 81% women; 51 +/- 12 y of age). Maintenance strategies included exercise and a calorie-restricted diet. Weight loss was analyzed by using an intention-to-treat analysis (baseline substitution). Results: After 1 y, mean (+/- SD) weight changes were -11.4 +/- 9.1 kg with the VLCD (18% dropout), -6.8 +/- 6.4 kg with the LCD (23% dropout), and -5.1 +/- 5.9 kg with the restricted normal-food diet (26% dropout). In an adjusted analysis, the VLCD group lost 2.8 kg (95% CI: 2.5, 3.2) and 3.8 kg (95% CI: 3.2, 4.5) more than did the LCD and restricted normal-food groups, respectively. A high baseline HMI and rapid initial weight loss were both independently associated with greater 1-y weight loss (P < 0.001). Younger age and low initial weight loss predicted an increased dropout rate (P < 0.001). Treatment of depression (OR: 1.4; 95% CI: 1.1, 1.9) and psychosis (OR: 2.6; 95% CI: 1.1, 6.3) were associated with an increased dropout rate in the VLCD group. Conclusion: A commercial weight-loss program, particularly one using a VLCD, was effective at reducing body weight in self-selected, self-paying adults.

  • 98.
    Ho, C. L. B.
    et al.
    Univ Tasmania, Hobart, Tas, Australia..
    Doust, J.
    Bond Univ, Gold Coast, Qld, Australia..
    Jackson, R.
    Univ Auckland, Auckland, New Zealand..
    McManus, R. J.
    Univ Oxford, Oxford OX1 2JD, England..
    Reid, C. M.
    Monash Univ, Clayton, Vic, Australia.;Curtin Univ, Perth, WA 6845, Australia..
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Nelson, M. R.
    Univ Tasmania, Hobart, Tas, Australia..
    Should You Leave A Legacy?: Potential Effects Of Delayed Blood Pressure Lowering Pharmacotherapy In Individuals Stratified By Absolute Cardiovascular Disease Risk2016Inngår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 67, nr 5, s. E17-E18Artikkel i tidsskrift (Annet vitenskapelig)
  • 99. Holmes, Michael V.
    et al.
    Dale, Caroline E.
    Zuccolo, Luisa
    Silverwood, Richard J.
    Guo, Yiran
    Ye, Zheng
    Prieto-Merino, David
    Dehghan, Abbas
    Trompet, Stella
    Wong, Andrew
    Cavadino, Alana
    Drogan, Dagmar
    Padmanabhan, Sandosh
    Li, Shanshan
    Yesupriya, Ajay
    Leusink, Maarten
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Hubacek, Jaroslav A.
    Pikhart, Hynek
    Swerdlow, Daniel I.
    Panayiotou, Andrie G.
    Borinskaya, Svetlana A.
    Finan, Chris
    Shah, Sonia
    Kuchenbaecker, Karoline B.
    Shah, Tina
    Engmann, Jorgen
    Folkersen, Lasse
    Eriksson, Per
    Ricceri, Fulvio
    Melander, Olle
    Sacerdote, Carlotta
    Gamble, Dale M.
    Rayaprolu, Sruti
    Ross, Owen A.
    McLachlan, Stela
    Vikhireva, Olga
    Sluijs, Ivonne
    Scott, Robert A.
    Adamkova, Vera
    Flicker, Leon
    Van Bockxmeer, Frank M.
    Power, Christine
    Marques-Vidal, Pedro
    Meade, Tom
    Marmot, Michael G.
    Ferro, Jose M.
    Paulos-Pinheiro, Sofia
    Humphries, Steve E.
    Talmud, Philippa J.
    Leach, Irene Mateo
    Verweij, Niek
    Linneberg, Allan
    Skaaby, Tea
    Doevendans, Pieter A.
    Cramer, Maarten J.
    Van der Harst, Pim
    Klungel, Olaf H.
    Dowling, Nicole F.
    Dominiczak, Anna F.
    Kumari, Meena
    Nicolaides, Andrew N.
    Weikert, Cornelia
    Boeing, Heiner
    Ebrahim, Shah
    Gaunt, Tom R.
    Price, Jackie F.
    Lannfelt, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Peasey, Anne
    Kubinova, Ruzena
    Pajak, Andrzej
    Malyutina, Sofia
    Voevoda, Mikhail I.
    Tamosiunas, Abdonas
    Maitland-van der Zee, Anke H.
    Norman, Paul E.
    Hankey, Graeme J.
    Bergmann, Manuela M.
    Hofman, Albert
    Franco, Oscar H.
    Cooper, Jackie
    Palmen, Jutta
    Spiering, Wilko
    de Jong, Pim A.
    Kuh, Diana
    Hardy, Rebecca
    Uitterlinden, Andre G.
    Ikram, M. Arfan
    Ford, Ian
    Hyppoenen, Elina
    Almeida, Osvaldo P.
    Wareham, Nicholas J.
    Khaw, Kay-Tee
    Hamsten, Anders
    Husemoen, Lise Lotte N.
    Tjonneland, Anne
    Tolstrup, Janne S.
    Rimm, Eric
    Beulens, Joline W. J.
    Verschuren, W. M. Monique
    Onland-Moret, N. Charlotte
    Hofker, Marten H.
    Wannamethee, S. Goya
    Whincup, Peter H.
    Morris, Richard
    Vicente, Astrid M.
    Watkins, Hugh
    Farrall, Martin
    Jukema, J. Wouter
    Meschia, James
    Cupples, L. Adrienne
    Sharp, Stephen J.
    Fornage, Myriam
    Kooperberg, Charles
    LaCroix, Andrea Z.
    Dai, James Y.
    Lanktree, Matthew B.
    Siscovick, David S.
    Jorgenson, Eric
    Spring, Bonnie
    Coresh, Josef
    Li, Yun R.
    Buxbaum, Sarah G.
    Schreiner, Pamela J.
    Ellison, R. Curtis
    Tsai, Michael Y.
    Patel, Sanjay R.
    Redline, Susan
    Johnson, Andrew D.
    Hoogeveen, Ron C.
    Rotter, Jerome I.
    Boerwinkle, Eric
    de Bakker, Paul I. W.
    Kivimaki, Mika
    Asselbergs, Folkert W.
    Sattar, Naveed
    Lawlor, Debbie A.
    Whittaker, John
    Smith, George Davey
    Mukamal, Kenneth
    Psaty, Bruce M.
    Wilson, James G.
    Lange, Leslie A.
    Hamidovic, Ajna
    Hingorani, Aroon D.
    Nordestgaard, Borge G.
    Bobak, Martin
    Leon, David A.
    Langenberg, Claudia
    Palmer, Tom M.
    Reiner, Alex P.
    Keating, Brendan J.
    Dudbridge, Frank
    Casas, Juan P.
    Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data2014Inngår i: BMJ-BRIT MED J, ISSN 1756-1833, Vol. 349, s. g4164-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective To use the rs1229984 variant in the alcohol dehydrogenase 1B gene (ADH1B) as an instrument to investigate the causal role of alcohol in cardiovascular disease. Design Mendelian randomisation meta-analysis of 56 epidemiological studies. Participants 261 991 individuals of European descent, including 20 259 coronary heart disease cases and 10 164 stroke events. Data were available on ADH1B rs1229984 variant, alcohol phenotypes, and cardiovascular biomarkers. Main outcome measures Odds ratio for coronary heart disease and stroke associated with the ADH1B variant in all individuals and by categories of alcohol consumption. Results Carriers of the A-allele of ADH1B rs1229984 consumed 17.2% fewer units of alcohol per week (95% confidence interval 15.6% to 18.9%), had a lower prevalence of binge drinking (odds ratio 0.78 (95% CI 0.73 to 0.84)), and had higher abstention (odds ratio 1.27 (1.21 to 1.34)) than non-carriers. Rs1229984 A-allele carriers had lower systolic blood pressure (-0.88 (-1.19 to -0.56) mm Hg), interleukin-6 levels (-5.2% (-7.8 to -2.4%)), waist circumference (-0.3 (-0.6 to -0.1) cm), and body mass index (-0.17 (-0.24 to -0.10) kg/m(2)). Rs1229984 A-allele carriers had lower odds of coronary heart disease (odds ratio 0.90 (0.84 to 0.96)). The protective association of the ADH1B rs1229984 A-allele variant remained the same across all categories of alcohol consumption (P= 0.83 for heterogeneity). Although no association of rs1229984 was identified with the combined subtypes of stroke, carriers of the A-allele had lower odds of ischaemic stroke (odds ratio 0.83 (0.72 to 0.95)). Conclusions Individuals with a genetic variant associated with non-drinking and lower alcohol consumption had a more favourable cardiovascular profile and a reduced risk of coronary heart disease than those without the genetic variant. This suggests that reduction of alcohol consumption, even for light to moderate drinkers, is beneficial for cardiovascular health.

  • 100.
    Huang, Biying
    et al.
    Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, 300 Pasteur Dr, Stanford, CA 94304 USA.;Karolinska Inst, Dept Med, S-17176 Stockholm, Sweden..
    Svensson, Per
    Karolinska Inst, Dept Med, S-17176 Stockholm, Sweden..
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Dalarna Univ, Sch Hlth & Social Studies, S-79188 Falun, Sweden..
    Sundstrom, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, 300 Pasteur Dr, Stanford, CA 94304 USA.
    Effects of cigarette smoking on cardiovascular-related protein profiles in two community-based cohort studies2016Inngår i: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 254, s. 52-58Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and aims: Cardiovascular diseases account for the largest fraction of smoking-induced deaths. Studies of smoking in relation to cardiovascular-related protein markers can provide novel insights into the biological effects of smoking. We investigated the associations between cigarette smoking and 80 protein markers known to be related to cardiovascular diseases in two community-based cohorts, the Prospective Study of the Vasculature in Uppsala Seniors (PIVUS, n = 969, 50% women, all aged 70 years) and the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 717, all men aged 77 years). Methods: Smoking status was self-reported and defined as current smoker, former smoker or never-smoker. Levels of the 80 proteins were measured using the proximity extension assay, a novel PCR-based proteomics technique. Results: We found 30 proteins to be significantly associated with current cigarette smoking in PIVUS (FDR<5%); and ten were replicated in ULSAM (p<0.05). Matrix metalloproteinase-12 (MMP-12), growth/differentiation factor 15 (GDF-15), urokinase plasminogen activator surface receptor (uPAR), TNF-related apoptosis-inducing ligand receptor 2 (TRAIL-R2), lectin-like oxidized LDL receptor 1 (LOX-1), hepatocyte growth factor (HGF), matrix metalloproteinase-10 (MMP-10) and matrix metalloproteinase-1 (MMP-1) were positively associated, while endothelial cell-specific molecule 1 (ESM-1) and interleukin-27 subunit alpha (IL27-A) showed inverse associations. All of them remained significant in a subset of individuals without manifest cardiovascular disease. Conclusions: The findings of the present study suggest that cigarette smoking may interfere with several essential parts of the atherosclerosis process, as evidenced by associations with protein markers representing endothelial dysfunction, inflammation, neointimal formation, foam cell formation and plaque instability. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

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