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198 results on '"Jansson, Jh"'

1. Positive predictive value and misclassification of diagnosis of pulmonary embolism and deep vein thrombosis in Swedish patient registries

Author: Öhman L, Johansson M, Jansson JH, Lind M, and Johansson L
Subjects: Pulmonary embolism, deep vein thrombosis, positive predictive value, International Classification of Diseases, validation, Infectious and parasitic diseases, RC109-216
Abstract: Ludvig Öhman, Magdalena Johansson, Jan-Håkan Jansson, Marcus Lind, Lars Johansson Department of Public Health and Clinical Medicine, Skellefteå Research Unit, Umeå University, Umeå, Västerbotten, Sweden Purpose: To validate diagnoses of pulmonary embolism (PE) and deep vein thrombosis (DVT) in administrative registries. We also estimated the frequency of misclassified PE and DVT events.Patients and methods: A registry search for ICD codes representing PE and DVT was performed between 1985 and 2014 in a large population-based cohort in northern Sweden. An additional search using an extended set of ICD codes was performed to identify misclassified events. Diagnoses were validated manually by reviewing medical records and radiology reports.Results: Searching ICD codes in the National Patient Registry and Cause of Death Registry identified 2,450 participants with a first-time diagnosis of PE or DVT. The positive predictive value (PPV) for a diagnosis of PE or DVT was 80.7% and 59.2%, respectively. For the period of 2009 to 2014, the PPV was higher for PE (85.8%) but lower for DVT (54.1%). Misclassification occurred in 16.4% of DVT events and 1.1% of PE events.Conclusion: Registry-based data on PE, especially in recent years, are of acceptable quality and can be considered for use in registry-based studies. For DVT, we found that data were of low quality in regards to both PPV and misclassification and should not be used without validation. Keywords: pulmonary embolism, deep vein thrombosis, positive predictive value, International Classification of Diseases, validation
Published: 2018

2. Incidence, type of atrial fibrillation and risk factors for stroke: a population-based cohort study

Author: Johansson C, Dahlqvist E, Andersson J, Jansson JH, and Johansson L
Subjects: atrial fibrillation, atrial flutter, incidence, risk factors for stroke, Infectious and parasitic diseases, RC109-216
Abstract: Cecilia Johansson, Erik Dahlqvist, Jonas Andersson, Jan-Håkan Jansson, Lars Johansson Department of Public Health and Clinical Medicine, Skellefteå Research Unit, Umeå University, Umeå, Västerbotten, Sweden Purpose: The aims of this study were to estimate the incidence of atrial fibrillation and atrial flutter (AF), to assess the presence of provoking factors and risk factors for stroke and systemic embolism, and to determine the type of AF in patients with first-diagnosed AF. Patients and methods: This cohort study was performed in northern Sweden between January 1, 2011 and December 31, 2012. Diagnosis registries were searched for the International Classification of Diseases-10 code for AF (I48) to identify cases of incident AF. All AF diagnoses were electrocardiogram-verified. Data pertaining to provoking factors, type of AF and presence of risk factors for stroke and systemic embolism according to the CHA2DS2-VASc score were obtained from medical records. Results: The incidence of AF in the entire population was 4.0 per 1,000 person-years. The incidence was 27.5 per 1,000 person-years in patients aged ≥80 years. A total of 21% of all patients had a provoking factor in association with the first-diagnosed episode of AF. The CHA2DS2-VASc score was 2 or higher in 81% of the patients. Permanent AF was the most common type of AF (29%). Conclusion: There was a considerable increase in the incidence of AF with age, and a provoking factor was found in one-fifth. The most common type of AF was permanent AF. Four in five patients had a CHA2DS2-VASc score of 2 or more. Keywords: atrial fibrillation, atrial flutter, incidence, risk factors for stroke
Published: 2017

3. Estimating the prevalence of atrial fibrillation in a general population using validated electronic health data

Author: Norberg J, Bäckström S, Jansson JH, and Johansson L
Subjects: Infectious and parasitic diseases, RC109-216
Abstract: Johannes Norberg, Svante Bäckström, Jan-Håkan Jansson, Lars JohanssonDepartment of Public Health and Clinical Medicine, Umeå University, Umeå, SwedenBackground: The purpose of this study was to determine the prevalence of atrial fibrillation (AF) in the general population and to validate an administrative diagnosis register, ie, the National Patient Register (NPR), and an electrocardiography (ECG) database in estimating disease prevalence.Methods: The study was conducted in a well defined region in northern Sweden (population n=75,945) which consists of one hospital and eleven primary health care centers. Subjects with AF were identified by searching the combined inpatient and outpatient International Classification of Diseases (ICD)-based NPR (ICD-10 code I48) and an ECG database with computer-interpreted AF from January 1, 2004 to December 31, 2010. All identified cases with AF were validated.Results: AF was confirmed in 2,274 patients. The overall prevalence was 3.0% (3.4% in men and 2.6% in women). AF prevalence rose steadily with age, and was 16.8% in patients aged 75 years and older and 21.9% in patients 85 years and older. Of all patients with validated AF, the NPR identified 93.2%. The ECG database identified an additional 6.8%, of which 81% were over 70 years of age. According to the NPR, the proportion of false positives and false negatives was 3.5% and 6.8%, respectively. The corresponding figure for the ECG database was 11.3% and 9.2%, respectively.Conclusion: Our study shows a high prevalence of AF, especially among the elderly. Searching the ECG database enhanced the detection of AF. The reliability of the NPR was high, with a relatively low proportion of false positives and negatives.Keywords: atrial fibrillation, epidemiology, prevalence
Published: 2013

4. Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality: An Individual-Level Pooled Analysis of 30 Cohort Studies

Author: Marklund, M, Wu, JHY, Imamura, F, Del Gobbo, LC, Fretts, A, De Goede, J, Shi, P, Tintle, N, Wennberg, M, Aslibekyan, S, Chen, TA, De Oliveira Otto, MC, Hirakawa, Y, Eriksen, HH, Kröger, J, Laguzzi, F, Lankinen, M, Murphy, RA, Prem, K, Samieri, C, Virtanen, J, Wood, AC, Wong, K, Yang, WS, Zhou, X, Baylin, A, Boer, JMA, Brouwer, IA, Campos, H, Chaves, PHM, Chien, KL, De Faire, U, Djoussé, L, Eiriksdottir, G, El-Abbadi, N, Forouhi, NG, Michael Gaziano, J, Geleijnse, JM, Gigante, B, Giles, G, Guallar, E, Gudnason, V, Harris, T, Harris, WS, Helmer, C, Hellenius, ML, Hodge, A, Hu, FB, Jacques, PF, Jansson, JH, Kalsbeek, A, Khaw, KT, Koh, WP, Laakso, M, Leander, K, Lin, HJ, Lind, L, Luben, R, Luo, J, Mcknight, B, Mursu, J, Ninomiya, T, Overvad, K, Psaty, BM, Rimm, E, Schulze, MB, Siscovick, D, Skjelbo Nielsen, M, Smith, AV, Steffen, BT, Steffen, L, Sun, Q, Sundström, J, Tsai, MY, Tunstall-Pedoe, H, Uusitupa, MIJ, Van Dam, RM, Veenstra, J, Monique Verschuren, WM, Wareham, N, Willett, W, Woodward, M, Yuan, JM, Micha, R, Lemaitre, RN, Mozaffarian, D, Risérus, U, Marklund, M, Wu, JHY, Imamura, F, Del Gobbo, LC, Fretts, A, De Goede, J, Shi, P, Tintle, N, Wennberg, M, Aslibekyan, S, Chen, TA, De Oliveira Otto, MC, Hirakawa, Y, Eriksen, HH, Kröger, J, Laguzzi, F, Lankinen, M, Murphy, RA, Prem, K, Samieri, C, Virtanen, J, Wood, AC, Wong, K, Yang, WS, Zhou, X, Baylin, A, Boer, JMA, Brouwer, IA, Campos, H, Chaves, PHM, Chien, KL, De Faire, U, Djoussé, L, Eiriksdottir, G, El-Abbadi, N, Forouhi, NG, Michael Gaziano, J, Geleijnse, JM, Gigante, B, Giles, G, Guallar, E, Gudnason, V, Harris, T, Harris, WS, Helmer, C, Hellenius, ML, Hodge, A, Hu, FB, Jacques, PF, Jansson, JH, Kalsbeek, A, Khaw, KT, Koh, WP, Laakso, M, Leander, K, Lin, HJ, Lind, L, Luben, R, Luo, J, Mcknight, B, Mursu, J, Ninomiya, T, Overvad, K, Psaty, BM, Rimm, E, Schulze, MB, Siscovick, D, Skjelbo Nielsen, M, Smith, AV, Steffen, BT, Steffen, L, Sun, Q, Sundström, J, Tsai, MY, Tunstall-Pedoe, H, Uusitupa, MIJ, Van Dam, RM, Veenstra, J, Monique Verschuren, WM, Wareham, N, Willett, W, Woodward, M, Yuan, JM, Micha, R, Lemaitre, RN, Mozaffarian, D, and Risérus, U
Abstract: Background: Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies. Methods: We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance-weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available). Results: In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15 198 incident cardiovascular events occurred among 68 659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88-0.99), 0.78 (0.70-0.85), and 0.88 (0.79-0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88-1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extrem
Published: 2019

5. Major lipids, apolipoproteins, and risk of vascular disease

Author: Emerging Risk Factors Collaboration, Di Angelantonio E, Sarwar N, Perry P, Kaptoge S, Ray KK, Thompson A, Wood AM, Lewington S, Sattar N, Packard CJ, Collins R, Thompson SG, Tipping RW, Ford CE, Pressel SL, Walldius G, Jungner I, Folsom AR, Chambless LE, Panagiotakos DB, Pitsavos C, Chrysohoou C, Stefanadis C, Knuiman M, Goldbourt U, Benderly M, Tanne D, Whincup PH, Wannamethee SG, Morris RW, Kiechl S, Willeit J, Santer P, Mayr A, Wald N, Ebrahim S, Lawlor DA, Yarnell JW, Gallacher J, Casiglia E, Tikhonoff V, Nietert PJ, Sutherland SE, Bachman DL, Keil JE, Cushman M, Psaty BM, Tracy RP, Tybjaerg Hansen A, Nordestgaard BG, Benn M, Frikke Schmidt R, Giampaoli S, Palmieri L, Vanuzzo D, Pilotto L, Gómez de la Cámara A, Gómez Gerique JA, Simons L, McCallum J, Friedlander Y, Fowkes FG, Lee AJ, Smith FB, Taylor J, Guralnik JM, Phillips CL, Wallace R, Guralnik J, Blazer DG, Khaw KT, Brenner H, Raum E, Müller H, Rothenbacher D, Jansson JH, Wennberg P, Nissinen A, Donfrancesco C, Salomaa V, Harald K, Jousilahti P, Vartiainen E, Woodward M, D'Agostino RB, Wolf PA, Vasan RS, Pencina MJ, Bladbjerg EM, Jørgensen T, Møller L, Jespersen J, Dankner R, Chetrit A, Lubin F, Rosengren A, Wilhelmsen L, Lappas G, Eriksson H, Björkelund C, Lissner L, Bengtsson C, Cremer P, Nagel D, Tilvis RS, Strandberg TE, Rodriguez B, Dekker JM, Nijpels G, Stehouwer CD, Rimm E, Pai JK, Sato S, Iso H, Kitamura A, Noda H, Salonen JT, Nyyssönen K, Tuomainen TP, Deeg DJ, Poppelaars JL, Meade TW, Cooper JA, Hedblad B, Berglund G, Engstrom G, Verschuren WM, Blokstra A, Döring A, Koenig W, Meisinger C, Mraz W, Verschure WM, Bas Bueno de Mesquita H, Kuller LH, Grandits G, Selmer R, Tverdal A, Nystad W, Gillum R, Mussolino M, Hankinson S, Manson J, Knottenbelt C, Bauer KA, Naito Y, Holme I, Nakagawa H, Miura K, Ducimetiere P, Jouven X, Crespo CJ, Garcia Palmieri MR, Amouyel P, Arveiler D, Evans A, Ferrieres J, Schulte H, Assmann G, Shepherd J, Ford I, Cantin B, Lamarche B, Després JP, Dagenais GR, Barrett Connor E, Wingard DL, Bettencourt R, Gudnason V, Aspelund T, Sigurdsson G, Thorsson B, Trevisan M, Witteman J, Kardys I, Breteler M, Hofman A, Tunstall Pedoe H, Tavendale R, Lowe GD, Howard BV, Zhang Y, Best L, Umans J, Ben Shlomo Y, Davey Smith G, Onat A, Njølstad I, Mathiesen EB, Løchen ML, Wilsgaard T, Ingelsson E, Lind L, Giedraitis V, Lannfelt L, Gaziano JM, Stampfer M, Ridker P, Ulmer H, Diem G, Concin H, Tosetto A, Rodeghiero F, Marmot M, Clarke R, Fletcher A, Brunner E, Shipley M, Buring J, Cobbe SM, Robertson M, He Y, Marin Ibañez A, Feskens EJ, Kromhout D, Walker M, Watson S, Erqou S, Orfei L, Pennells L, Perry PL, Alexander M, Wensley F, White IR, Danesh J., PANICO, SALVATORE, Developmental Genetics, EMGO+ - Lifestyle, Overweight and Diabetes, Epidemiology and Data Science, General practice, Psychiatry, EMGO - Lifestyle, overweight and diabetes, Emerging Risk Factors, Collaboration, Di Angelantonio, E, Sarwar, N, Perry, P, Kaptoge, S, Ray, Kk, Thompson, A, Wood, Am, Lewington, S, Sattar, N, Packard, Cj, Collins, R, Thompson, Sg, Tipping, Rw, Ford, Ce, Pressel, Sl, Walldius, G, Jungner, I, Folsom, Ar, Chambless, Le, Panagiotakos, Db, Pitsavos, C, Chrysohoou, C, Stefanadis, C, Knuiman, M, Goldbourt, U, Benderly, M, Tanne, D, Whincup, Ph, Wannamethee, Sg, Morris, Rw, Kiechl, S, Willeit, J, Santer, P, Mayr, A, Wald, N, Ebrahim, S, Lawlor, Da, Yarnell, Jw, Gallacher, J, Casiglia, E, Tikhonoff, V, Nietert, Pj, Sutherland, Se, Bachman, Dl, Keil, Je, Cushman, M, Psaty, Bm, Tracy, Rp, Tybjaerg Hansen, A, Nordestgaard, Bg, Benn, M, Frikke Schmidt, R, Giampaoli, S, Palmieri, L, Panico, Salvatore, Vanuzzo, D, Pilotto, L, Gómez de la Cámara, A, Gómez Gerique, Ja, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, Aj, Smith, Fb, Taylor, J, Guralnik, Jm, Phillips, Cl, Wallace, R, Guralnik, J, Blazer, Dg, Khaw, Kt, Brenner, H, Raum, E, Müller, H, Rothenbacher, D, Jansson, Jh, Wennberg, P, Nissinen, A, Donfrancesco, C, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, Woodward, M, D'Agostino, Rb, Wolf, Pa, Vasan, R, Pencina, Mj, Bladbjerg, Em, Jørgensen, T, Møller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Rosengren, A, Wilhelmsen, L, Lappas, G, Eriksson, H, Björkelund, C, Lissner, L, Bengtsson, C, Cremer, P, Nagel, D, Tilvis, R, Strandberg, Te, Rodriguez, B, Dekker, Jm, Nijpels, G, Stehouwer, Cd, Rimm, E, Pai, Jk, Sato, S, Iso, H, Kitamura, A, Noda, H, Salonen, Jt, Nyyssönen, K, Tuomainen, Tp, Deeg, Dj, Poppelaars, Jl, Meade, Tw, Cooper, Ja, Hedblad, B, Berglund, G, Engstrom, G, Verschuren, Wm, Blokstra, A, Döring, A, Koenig, W, Meisinger, C, Mraz, W, Verschure, Wm, Bas Bueno de Mesquita, H, Kuller, Lh, Grandits, G, Selmer, R, Tverdal, A, Nystad, W, Gillum, R, Mussolino, M, Hankinson, S, Manson, J, Knottenbelt, C, Bauer, Ka, Naito, Y, Holme, I, Nakagawa, H, Miura, K, Ducimetiere, P, Jouven, X, Crespo, Cj, Garcia Palmieri, Mr, Amouyel, P, Arveiler, D, Evans, A, Ferrieres, J, Schulte, H, Assmann, G, Shepherd, J, Ford, I, Cantin, B, Lamarche, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Wingard, Dl, Bettencourt, R, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Witteman, J, Kardys, I, Breteler, M, Hofman, A, Tunstall Pedoe, H, Tavendale, R, Lowe, Gd, Howard, Bv, Zhang, Y, Best, L, Umans, J, Ben Shlomo, Y, Davey Smith, G, Onat, A, Njølstad, I, Mathiesen, Eb, Løchen, Ml, Wilsgaard, T, Ingelsson, E, Lind, L, Giedraitis, V, Lannfelt, L, Gaziano, Jm, Stampfer, M, Ridker, P, Ulmer, H, Diem, G, Concin, H, Tosetto, A, Rodeghiero, F, Marmot, M, Clarke, R, Fletcher, A, Brunner, E, Shipley, M, Buring, J, Cobbe, Sm, Robertson, M, He, Y, Marin Ibañez, A, Feskens, Ej, Kromhout, D, Walker, M, Watson, S, Erqou, S, Orfei, L, Pennells, L, Perry, Pl, Alexander, M, Wensley, F, White, Ir, and Danesh, J.
Subjects: medicine.medical_specialty, Apolipoprotein B, biology, Triglyceride, business.industry, Vascular disease, Cholesterol, Proportional hazards model, Hazard ratio, Context (language use), General Medicine, 11 Medical And Health Sciences, medicine.disease, Gastroenterology, Article, chemistry.chemical_compound, Endocrinology, chemistry, Internal medicine, General & Internal Medicine, biology.protein, Medicine, lipids (amino acids, peptides, and proteins), Myocardial infarction, business
Abstract: Udgivelsesdato: 2009-Nov-11 CONTEXT: Associations of major lipids and apolipoproteins with the risk of vascular disease have not been reliably quantified. OBJECTIVE: To assess major lipids and apolipoproteins in vascular risk. DESIGN, SETTING, AND PARTICIPANTS: Individual records were supplied on 302,430 people without initial vascular disease from 68 long-term prospective studies, mostly in Europe and North America. During 2.79 million person-years of follow-up, there were 8857 nonfatal myocardial infarctions, 3928 coronary heart disease [CHD] deaths, 2534 ischemic strokes, 513 hemorrhagic strokes, and 2536 unclassified strokes. MAIN OUTCOME MEASURES: Hazard ratios (HRs), adjusted for several conventional factors, were calculated for 1-SD higher values: 0.52 log(e) triglyceride, 15 mg/dL high-density lipoprotein cholesterol (HDL-C), 43 mg/dL non-HDL-C, 29 mg/dL apolipoprotein AI, 29 mg/dL apolipoprotein B, and 33 mg/dL directly measured low-density lipoprotein cholesterol (LDL-C). Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis. RESULTS: The rates of CHD per 1000 person-years in the bottom and top thirds of baseline lipid distributions, respectively, were 2.6 and 6.2 with triglyceride, 6.4 and 2.4 with HDL-C, and 2.3 and 6.7 with non-HDL-C. Adjusted HRs for CHD were 0.99 (95% CI, 0.94-1.05) with triglyceride, 0.78 (95% CI, 0.74-0.82) with HDL-C, and 1.50 (95% CI, 1.39-1.61) with non-HDL-C. Hazard ratios were at least as strong in participants who did not fast as in those who did. The HR for CHD was 0.35 (95% CI, 0.30-0.42) with a combination of 80 mg/dL lower non-HDL-C and 15 mg/dL higher HDL-C. For the subset with apolipoproteins or directly measured LDL-C, HRs were 1.50 (95% CI, 1.38-1.62) with the ratio non-HDL-C/HDL-C, 1.49 (95% CI, 1.39-1.60) with the ratio apo B/apo AI, 1.42 (95% CI, 1.06-1.91) with non-HDL-C, and 1.38 (95% CI, 1.09-1.73) with directly measured LDL-C. Hazard ratios for ischemic stroke were 1.02 (95% CI, 0.94-1.11) with triglyceride, 0.93 (95% CI, 0.84-1.02) with HDL-C, and 1.12 (95% CI, 1.04-1.20) with non-HDL-C. CONCLUSION: Lipid assessment in vascular disease can be simplified by measurement of either total and HDL cholesterol levels or apolipoproteins without the need to fast and without regard to triglyceride.
Published: 2016

6. Use of Repeated Blood Pressure and Cholesterol Measurements to Improve Cardiovascular Disease Risk Prediction: An Individual-Participant-Data Meta-Analysis

Author: Paige, E, Barrett, J, Pennells, L, Sweeting, M, Willeit, P, Di Angelantonio, E, Gudnason, V, Nordestgaard, BG, Psaty, BM, Goldbourt, U, Best, LG, Assmann, G, Salonen, JT, Nietert, PJ, Verschuren, WMM, Brunner, EJ, Kronmal, RA, Salomaa, V, Bakker, SJL, Dagenais, GR, Sato, S, Jansson, JH, Willeit, J, Onat, A, de la Camara, AG, Roussel, R, Volzke, H, Dankner, R, Tipping, RW, Meade, TW, Donfrancesco, C, Kuller, LH, Peters, A, Gallacher, J, Kromhout, D, Iso, H, Knuiman, M, Casiglia, E, Kavousi, Maryam, Palmieri, L, Sundstrom, J, Davis, BR, Njolstad, I, Couper, D, Danesh, J, Thompson, SG, Wood, A, Paige, E, Barrett, J, Pennells, L, Sweeting, M, Willeit, P, Di Angelantonio, E, Gudnason, V, Nordestgaard, BG, Psaty, BM, Goldbourt, U, Best, LG, Assmann, G, Salonen, JT, Nietert, PJ, Verschuren, WMM, Brunner, EJ, Kronmal, RA, Salomaa, V, Bakker, SJL, Dagenais, GR, Sato, S, Jansson, JH, Willeit, J, Onat, A, de la Camara, AG, Roussel, R, Volzke, H, Dankner, R, Tipping, RW, Meade, TW, Donfrancesco, C, Kuller, LH, Peters, A, Gallacher, J, Kromhout, D, Iso, H, Knuiman, M, Casiglia, E, Kavousi, Maryam, Palmieri, L, Sundstrom, J, Davis, BR, Njolstad, I, Couper, D, Danesh, J, Thompson, SG, and Wood, A
Published: 2017

7. A genomic approach to therapeutic target validation identifies a glucose-lowering GLP1R variant protective for coronary heart disease

Author: Scott, RA, Freitag, DF, Li, L, Chu, AY, Surendran, P, Young, R, Grarup, N, Stancáková, A, Chen, Y, Varga, TV, Yaghootkar, H, Luan, J, Zhao, JH, Willems, SM, Wessel, J, Wang, S, Maruthur, N, Michailidou, K, Pirie, A, Van Der Lee, SJ, Gillson, C, Al Olama, AA, Amouyel, P, Arriola, L, Arveiler, D, Aviles-Olmos, I, Balkau, B, Barricarte, A, Barroso, I, Garcia, SB, Bis, JC, Blankenberg, S, Boehnke, M, Boeing, H, Boerwinkle, E, Borecki, IB, Bork-Jensen, J, Bowden, S, Caldas, C, Caslake, M, Cupples, LA, Cruchaga, C, Czajkowski, J, Den Hoed, M, Dunn, JA, Earl, HM, Ehret, GB, Ferrannini, E, Ferrieres, J, Foltynie, T, Ford, I, Forouhi, NG, Gianfagna, F, Gonzalez, C, Grioni, S, Hiller, L, Jansson, JH, Jørgensen, ME, Jukema, JW, Kaaks, R, Kee, F, Kerrison, ND, Key, TJ, Kontto, J, Kote-Jarai, Z, Kraja, AT, Kuulasmaa, K, Kuusisto, J, Linneberg, A, Liu, C, Marenne, G, Mohlke, KL, Morris, AP, Muir, K, Müller-Nurasyid, M, Munroe, PB, and Navarro, C
Abstract: Copyright 2016 by the American Association for the Advancement of Science; all rights reserved. Regulatory authorities have indicated that new drugs to treat type 2 diabetes (T2D) should not be associated with an unacceptable increase in cardiovascular risk. Human genetics may be able to guide development of antidiabetic therapies by predicting cardiovascular and other health endpoints. We therefore investigated the association of variants in six genes that encode drug targets for obesity or T2D with a range of metabolic traits in up to 11, 806 individuals by targeted exome sequencing and follow-up in 39, 979 individuals by targeted genotyping, with additional in silico follow-up in consortia. We used these data to first compare associations of variants in genes encoding drug targets with the effects of pharmacological manipulation of those targets in clinical trials. We then tested the association of those variants with disease outcomes, including coronary heart disease, to predict cardiovascular safety of these agents. A low-frequency missense variant (Ala316Thr; rs10305492) in the gene encoding glucagon-like peptide-1 receptor (GLP1R), the target of GLP1R agonists, was associated with lower fasting glucose and T2D risk, consistent with GLP1R agonist therapies. The minor allele was also associated with protection against heart disease, thus providing evidence that GLP1R agonists are not likely to be associated with an unacceptable increase in cardiovascular risk. Our results provide an encouraging signal that these agents may be associated with benefit, a question currently being addressed in randomized controlled trials. Genetic variants associated with metabolic traits and multiple disease outcomes can be used to validate therapeutic targets at an early stage in the drug development process.
Published: 2016

8. Collaborative pooled analysis of data on C-reactive protein gene variants and coronary disease: judging causality by Mendelian randomisation

Author: Danesh, J, Collaborat, CRPCHDG, Hingorani, A, Wensley, F, Casas, JP, Smeeth, L, Samani, NJ, Hall, A, Whincup, P, Morris, R, Lawlor, DA, Smith, GD, Timpson, N, Ebrahim, S, Brown, M, Sandhu, M, Reiner, A, Psaty, B, Lange, L, Cushman, M, Tracy, R, Nordestgaard, BG, Tybjaerg-Hansen, A, Zacho, J, Hung, J, Thompson, P, Beilby, J, Palmer, LJ, Fowkes, G, Lowe, G, Tzoulaki, I, Kumari, M, Overvad, K, Khaw, KT, Benjamin, EJ, Larson, MG, Yamamoto, JF, Chiodini, B, Franzosi, M, Norman, PE, Hankey, GJ, Jamrozik, K, Palmer, L, Rimm, E, Pai, J, Heckbert, S, Bis, J, Yusuf, S, Anand, S, Engert, J, Collins, R, Melander, O, Berglund, G, Ladenvall, P, Johansson, L, Jansson, JH, Hallmans, G, Humphries, S, Manson, J, Saleheen, D, Frossard, P, Sattar, N, Robertson, M, Shepherd, J, Schaefer, E, Hofman, A, Witteman, JCM, Kardys, I, de Faire, U, Bennet, A, O'Reilly, D, McMahon, A, Packard, C, Clarke, R, Greenland, P, Bowden, J, Di Angelantonio, E, Shah, T, Verzilli, C, Walker, M, and Wittaker, J
Subjects: Research design, Pathology, medicine.medical_specialty, Heart disease, Epidemiology, Coronary Disease, Bioinformatics, medicine, Humans, Cooperative Behavior, Prospective cohort study, Inflammation, Polymorphism, Genetic, biology, business.industry, C-reactive protein, Haplotype, Case-control study, medicine.disease, Causality, C-Reactive Protein, Haplotypes, Research Design, Case-Control Studies, biology.protein, Cell activation, business
Abstract: Many prospective studies have reported associations between circulating C-reactive protein (CRP) levels and risk of coronary heart disease (CHD), but causality remains uncertain. Studies of CHD are being conducted that involve measurement of common polymorphisms of the CRP gene known to be associated with circulating concentrations, thereby utilising these variants as proxies for circulating CRP levels. By analysing data from several studies examining the association between relevant CRP polymorphisms and CHD risk, the present collaboration will undertake a Mendelian randomisation analysis to help assess the likelihood of any causal relevance of CRP levels to CHD risk. A central database is being established containing individual data on CRP polymorphisms, circulating CRP levels, and major coronary outcomes as well as age, sex and other relevant characteristics. Associations between CRP polymorphisms or haplotypes and CHD will be evaluated under different circumstances. This collaboration comprises, at present, about 37,000 CHD outcomes and about 120,000 controls, which should yield suitably precise findings to help judge causality. This work should advance understanding of the relevance of low-grade inflammation to CHD and indicate whether or not CRP itself is involved in long-term pathogenesis.
Published: 2008

9. Rare Functional Variant in TM2D3 is Associated with Late-Onset Alzheimer's Disease

Author: Jakobsdottir, J, van der Lee, Sven, Bis, JC, Chouraki, V, Li-Kroeger, D, Yamamoto, S, Grove, ML, Naj, A, Vronskaya, M, Salazar, JL, DeStefano, AL, Brody, JA, Smith, AV, Amin, Najaf, Sims, R, Verbaas, Carla, Choi, SH, Satizabal, CL, Lopez, OL, Beiser, A, Ikram, Arfan, Garcia, ME, Hayward, C, Varga, TV, Ripatti, S, Franks, PW, Hallmans, G, Rolandsson, O, Jansson, JH, Porteous, DJ, Salomaa, V, Eiriksdottir, G, Rice, KM, Bellen, HJ, Levy, D, Uitterlinden, André, Emilsson, V, Rotter, JI, Aspelund, T, O'Donnell, CJ, Fitzpatrick, AL, Launer, LJ, Hofman, Bert, Wang, LS (Li-San), Williams, J, Schellenberg, GD, Boerwinkle, E, Psaty, BM, Seshadri, S, Shulman, JM, Gudnason, V, Duijn, Cornelia, Jakobsdottir, J, van der Lee, Sven, Bis, JC, Chouraki, V, Li-Kroeger, D, Yamamoto, S, Grove, ML, Naj, A, Vronskaya, M, Salazar, JL, DeStefano, AL, Brody, JA, Smith, AV, Amin, Najaf, Sims, R, Verbaas, Carla, Choi, SH, Satizabal, CL, Lopez, OL, Beiser, A, Ikram, Arfan, Garcia, ME, Hayward, C, Varga, TV, Ripatti, S, Franks, PW, Hallmans, G, Rolandsson, O, Jansson, JH, Porteous, DJ, Salomaa, V, Eiriksdottir, G, Rice, KM, Bellen, HJ, Levy, D, Uitterlinden, André, Emilsson, V, Rotter, JI, Aspelund, T, O'Donnell, CJ, Fitzpatrick, AL, Launer, LJ, Hofman, Bert, Wang, LS (Li-San), Williams, J, Schellenberg, GD, Boerwinkle, E, Psaty, BM, Seshadri, S, Shulman, JM, Gudnason, V, and Duijn, Cornelia
Abstract: We performed an exome-wide association analysis in 1393 late-onset Alzheimer's disease (LOAD) cases and 8141 controls from the CHARGE consortium. We found that a rare variant (P155L) in TM2D3 was enriched in Icelanders (similar to 0.5% versus < 0.05% in other European populations). In 433 LOAD cases and 3903 controls from the Icelandic AGES substudy, P155L was associated with increased risk and earlier onset of LOAD [odds ratio (95% CI) = 7.5 (3.5-15.9), p = 6.6x10(-9)]. Mutation in the Drosophila TM2D3 homolog, almondex, causes a phenotype similar to loss of Notch/Presenilin signaling. Human TM2D3 is capable of rescuing these phenotypes, but this activity is abolished by P155L, establishing it as a functionally damaging allele. Our results establish a rare TM2D3 variant in association with LOAD susceptibility, and together with prior work suggests possible links to the beta-amyloid cascade.
Published: 2016

10. Fruit and vegetable intake and mortality fromischaemic heart disease: results from the European Prospective Investigation intoCancer and Nutrition (EPIC)-Heart study

Author: Crowe FL, Roddam AW, Key TJ, Appleby PN, Overvad K, Jakobsen MU, Tjønneland A, Hansen L, Boeing H, Weikert C, Linseisen J, Kaaks R, Trichopoulou A, Misirli G, Lagiou P, Sacerdote C, Pala V, Palli D, Tumino R, Bueno de Mesquita HB, Boer J, van Gils CH, Beulens JW, Barricarte A, Rodríguez L, Larrañaga N, Sánchez MJ, Tormo MJ, Buckland G, Lund E, Hedblad B, Melander O, Jansson JH, Wennberg P, Wareham NJ, Slimani N, Romieu I, Jenab M, Danesh J, Gallo V, Norat T, Riboli E, European Prospective Investigation into Cancer, Nutrition Heart Study C.o.l.l.a.b.o.r.a.t.o.r.s., PANICO, SALVATORE, Crowe, Fl, Roddam, Aw, Key, Tj, Appleby, Pn, Overvad, K, Jakobsen, Mu, Tjønneland, A, Hansen, L, Boeing, H, Weikert, C, Linseisen, J, Kaaks, R, Trichopoulou, A, Misirli, G, Lagiou, P, Sacerdote, C, Pala, V, Palli, D, Tumino, R, Panico, Salvatore, Bueno de Mesquita, Hb, Boer, J, van Gils, Ch, Beulens, Jw, Barricarte, A, Rodríguez, L, Larrañaga, N, Sánchez, Mj, Tormo, Mj, Buckland, G, Lund, E, Hedblad, B, Melander, O, Jansson, Jh, Wennberg, P, Wareham, Nj, Slimani, N, Romieu, I, Jenab, M, Danesh, J, Gallo, V, Norat, T, Riboli, E, European Prospective Investigation into, Cancer, and Nutrition Heart Study, C. o. l. l. a. b. o. r. a. t. o. r. s.
Published: 2011

11. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis

Author: Emerging Risk Factors Collaboration, Kaptoge S, Di Angelantonio E, Lowe G, Pepys MB, Thompson SG, Collins R, Danesh JTipping RW, Ford CE, Pressel SL, Walldius G, Jungner I, Folsom AR, Chambless L, Ballantyne CM, Panagiotakos D, Pitsavos C, Chrysohoou C, Stefanadis C, Knuiman MW, Goldbourt U, Benderly M, Tanne D, Whincup P, Wannamethee SG, Morris RW, Kiechl S, Willeit J, Mayr A, Schett G, Wald N, Ebrahim S, Lawlor D, Yarnell J, Gallacher J, Casiglia E, Tikhonoff V, Nietert PJ, Sutherland SE, Bachman DL, Keil JE, Cushman M, Psaty BM, Tracy R, Tybjaerg Hansen A, Nordestgaard BG, Zacho J, Frikke Schmidt R, Giampaoli S, Palmieri L, Vanuzzo D, Pilotto L, de la Cámara AG, Gerique JA, Simons L, McCallum J, Friedlander Y, Fowkes FG, Lee A, Taylor J, Guralnik JM, Phillips CL, Wallace RB, Blazer DG, Khaw KT, Brenner H, Raum E, Müller H, Rothenbacher D, Jansson JH, Wennberg P, Nissinen A, Donfrancesco C, Salomaa V, Harald K, Jousilahti P, Vartiainen E, Woodward M, D'Agostino RB, Wolf PA, Vasan RS, Benjamin EJ, Bladbjerg EM, Jørgensen T, Møller L, Jespersen J, Dankner R, Chetrit A, Lubin F, Rosengren A, Wilhelmsen L, Lappas G, Eriksson H, Björkelund C, Lissner L, Bengtsson C, Cremer P, Nagel D, Tilvis RS, Strandberg TE, Kiyohara Y, Arima H, Doi Y, Ninomiya T, Rodriguez B, Dekker J, Nijpels G, Stehouwer CD, Rimm E, Pai JK, Sato S, Iso H, Kitamura A, Noda H, Salonen JT, Nyyssönen K, Tuomainen TP, Laukkanen JA, Deeg DJ, Bremmer MA, Meade TW, Cooper JA, Hedblad B, Berglund G, Engström G, Verschuren WM, Blokstra A, Shea S, Döring A, Koenig W, Meisinger C, Bueno de Mesquita HB, Kuller LH, Grandits G, Selmer R, Tverdal A, Nystad W, Gillum RF, Mussolino M, Hankinson S, Manson JE, Knottenbelt C, Bauer KA, Davidson K, Kirkland S, Shaffer J, Korin MR, Naito Y, Holme I, Nakagawa H, Miura K, Ducimetiere P, Jouven X, Luc G, Crespo CJ, Garcia Palmieri MR, Amouyel P, Arveiler D, Evans A, Ferrieres J, Schulte H, Assmann G, Packard CJ, Sattar N, Westendorp RG, Buckley BM, Cantin B, Lamarche B, Després JP, Dagenais GR, Barrett Connor E, Wingard DL, Bettencourt RR, Gudnason V, Aspelund T, Sigurdsson G, Thorsson B, Trevisan M, Witteman J, Kardys I, Breteler MM, Hofman A, Tunstall Pedoe H, Tavendale R, Howard BV, Zhang Y, Best L, Umans J, Ben Shlomo Y, Davey Smith G, Onat A, Njølstad I, Mathiesen EB, Løchen ML, Wilsgaard T, Ingelsson E, Basu S, Cederholm T, Byberg L, Gaziano JM, Stampfer M, Ridker PM, Ulmer H, Diem G, Concin H, Tosetto A, Rodeghiero F, Wassertheil Smoller S, Marmot IM, Clarke R, Fletcher A, Brunner E, Shipley M, Buring J, Shepherd J, Cobbe S, Ford I, Robertson M, He Y, Ibañez AM, Feskens EJ, Walker M, Watson S, Erqou S, Lewington S, Pennells L, Perry PL, Ray KK, Sarwar N, Alexander M, Thompson A, White IR, Wood AM, Danesh J., PANICO, SALVATORE, Interne Geneeskunde, MUMC+: MA Interne Geneeskunde (3), RS: CARIM School for Cardiovascular Diseases, General practice, EMGO - Lifestyle, overweight and diabetes, Psychiatry, EMGO - Mental health, Emerging Risk Factors, Collaboration, Kaptoge, S, Di Angelantonio, E, Lowe, G, Pepys, Mb, Thompson, Sg, Collins, R, Danesh JTipping, Rw, Ford, Ce, Pressel, Sl, Walldius, G, Jungner, I, Folsom, Ar, Chambless, L, Ballantyne, Cm, Panagiotakos, D, Pitsavos, C, Chrysohoou, C, Stefanadis, C, Knuiman, Mw, Goldbourt, U, Benderly, M, Tanne, D, Whincup, P, Wannamethee, Sg, Morris, Rw, Kiechl, S, Willeit, J, Mayr, A, Schett, G, Wald, N, Ebrahim, S, Lawlor, D, Yarnell, J, Gallacher, J, Casiglia, E, Tikhonoff, V, Nietert, Pj, Sutherland, Se, Bachman, Dl, Keil, Je, Cushman, M, Psaty, Bm, Tracy, R, Tybjaerg Hansen, A, Nordestgaard, Bg, Zacho, J, Frikke Schmidt, R, Giampaoli, S, Palmieri, L, Panico, Salvatore, Vanuzzo, D, Pilotto, L, de la Cámara, Ag, Gerique, Ja, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, A, Taylor, J, Guralnik, Jm, Phillips, Cl, Wallace, Rb, Blazer, Dg, Khaw, Kt, Brenner, H, Raum, E, Müller, H, Rothenbacher, D, Jansson, Jh, Wennberg, P, Nissinen, A, Donfrancesco, C, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, Woodward, M, D'Agostino, Rb, Wolf, Pa, Vasan, R, Benjamin, Ej, Bladbjerg, Em, Jørgensen, T, Møller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Rosengren, A, Wilhelmsen, L, Lappas, G, Eriksson, H, Björkelund, C, Lissner, L, Bengtsson, C, Cremer, P, Nagel, D, Tilvis, R, Strandberg, Te, Kiyohara, Y, Arima, H, Doi, Y, Ninomiya, T, Rodriguez, B, Dekker, J, Nijpels, G, Stehouwer, Cd, Rimm, E, Pai, Jk, Sato, S, Iso, H, Kitamura, A, Noda, H, Salonen, Jt, Nyyssönen, K, Tuomainen, Tp, Laukkanen, Ja, Deeg, Dj, Bremmer, Ma, Meade, Tw, Cooper, Ja, Hedblad, B, Berglund, G, Engström, G, Verschuren, Wm, Blokstra, A, Shea, S, Döring, A, Koenig, W, Meisinger, C, Bueno de Mesquita, Hb, Kuller, Lh, Grandits, G, Selmer, R, Tverdal, A, Nystad, W, Gillum, Rf, Mussolino, M, Hankinson, S, Manson, Je, Knottenbelt, C, Bauer, Ka, Davidson, K, Kirkland, S, Shaffer, J, Korin, Mr, Naito, Y, Holme, I, Nakagawa, H, Miura, K, Ducimetiere, P, Jouven, X, Luc, G, Crespo, Cj, Garcia Palmieri, Mr, Amouyel, P, Arveiler, D, Evans, A, Ferrieres, J, Schulte, H, Assmann, G, Packard, Cj, Sattar, N, Westendorp, Rg, Buckley, Bm, Cantin, B, Lamarche, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Wingard, Dl, Bettencourt, Rr, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Witteman, J, Kardys, I, Breteler, Mm, Hofman, A, Tunstall Pedoe, H, Tavendale, R, Howard, Bv, Zhang, Y, Best, L, Umans, J, Ben Shlomo, Y, Davey Smith, G, Onat, A, Njølstad, I, Mathiesen, Eb, Løchen, Ml, Wilsgaard, T, Ingelsson, E, Basu, S, Cederholm, T, Byberg, L, Gaziano, Jm, Stampfer, M, Ridker, Pm, Ulmer, H, Diem, G, Concin, H, Tosetto, A, Rodeghiero, F, Wassertheil Smoller, S, Marmot, Im, Clarke, R, Fletcher, A, Brunner, E, Shipley, M, Buring, J, Shepherd, J, Cobbe, S, Ford, I, Robertson, M, He, Y, Ibañez, Am, Feskens, Ej, Walker, M, Watson, S, Erqou, S, Lewington, S, Pennells, L, Perry, Pl, Ray, Kk, Sarwar, N, Alexander, M, Thompson, A, White, Ir, Wood, Am, and Danesh, J.
Subjects: Lung Diseases, Male, Databases, Factual, Plasma-fibrinogen, Blood Pressure, Coronary Disease, 030204 cardiovascular system & hematology, Associations, Body Mass Index, Low-density-lipoprotein, Leukocyte Count, 0302 clinical medicine, Risk Factors, Neoplasms, 030212 general & internal medicine, Stroke, Framingham Risk Score, biology, Smoking, 11 Medical And Health Sciences, General Medicine, Articles, Middle Aged, 3. Good health, C-Reactive Protein, Cholesterol, Regression Analysis, low-density lipoprotein cardiovascular-disease nonvascular mortality regression dilution plasma-fibrinogen mendelian randomization independent predictor prospective cohorts vascular-disease inflammation, Female, Risk assessment, medicine.medical_specialty, Alcohol Drinking, Regression dilution, Motor Activity, Risk Assessment, 03 medical and health sciences, Sex Factors, Cardiovascular-disease, General & Internal Medicine, Internal medicine, Diabetes Mellitus, medicine, Humans, Women, Risk factor, Serum Albumin, Triglycerides, Inflammation, Markers, Independent predictor, Interleukin-6, business.industry, Vascular disease, C-reactive protein, Fibrinogen, medicine.disease, Surgery, Relative risk, biology.protein, Nonvascular mortality, business, Biomarkers
Abstract: Udgivelsesdato: 2010-Jan-9 BACKGROUND: Associations of C-reactive protein (CRP) concentration with risk of major diseases can best be assessed by long-term prospective follow-up of large numbers of people. We assessed the associations of CRP concentration with risk of vascular and non-vascular outcomes under different circumstances. METHODS: We meta-analysed individual records of 160 309 people without a history of vascular disease (ie, 1.31 million person-years at risk, 27 769 fatal or non-fatal disease outcomes) from 54 long-term prospective studies. Within-study regression analyses were adjusted for within-person variation in risk factor levels. RESULTS: Log(e) CRP concentration was linearly associated with several conventional risk factors and inflammatory markers, and nearly log-linearly with the risk of ischaemic vascular disease and non-vascular mortality. Risk ratios (RRs) for coronary heart disease per 1-SD higher log(e) CRP concentration (three-fold higher) were 1.63 (95% CI 1.51-1.76) when initially adjusted for age and sex only, and 1.37 (1.27-1.48) when adjusted further for conventional risk factors; 1.44 (1.32-1.57) and 1.27 (1.15-1.40) for ischaemic stroke; 1.71 (1.53-1.91) and 1.55 (1.37-1.76) for vascular mortality; and 1.55 (1.41-1.69) and 1.54 (1.40-1.68) for non-vascular mortality. RRs were largely unchanged after exclusion of smokers or initial follow-up. After further adjustment for fibrinogen, the corresponding RRs were 1.23 (1.07-1.42) for coronary heart disease; 1.32 (1.18-1.49) for ischaemic stroke; 1.34 (1.18-1.52) for vascular mortality; and 1.34 (1.20-1.50) for non-vascular mortality. INTERPRETATION: CRP concentration has continuous associations with the risk of coronary heart disease, ischaemic stroke, vascular mortality, and death from several cancers and lung disease that are each of broadly similar size. The relevance of CRP to such a range of disorders is unclear. Associations with ischaemic vascular disease depend considerably on conventional risk factors and other markers of inflammation. FUNDING: British Heart Foundation, UK Medical Research Council, BUPA Foundation, and GlaxoSmithKline.
Published: 2010

12. Emerging Risk Factors Collaboration. Statistical methods for the time-to-event analysis of individual participant data from multiple epidemiological studies

Author: hompson S, Kaptoge S, White I, Wood A, Thompson SG, White IR, Wood AM, Perry PL, Danesh J, Tipping RW, Ford CE, Simpson LM, Walldius G, Jungner I, Chambless LE, Panagiotakos DB, Pitsavos C, Chrysohoou C, Stefanadis C, Knuiman M, Goldbourt U, Benderly M, Tanne D, Whincup PH, Wannamethee SG, Morris RW, Willeit J, Kiechl S, Santer P, Mayr A, Lawlor DA, Yarnell JW, Gallacher J, Casiglia E, Tikhonoff V, Nietert PJ, Sutherland SE, Bachman DL, Keil JE, Cushman M, Tracy RP, Tybjærg Hansen A, Nordestgaard BG, Benn M, Frikke Schmidt R, Giampaoli S, Palmieri L, Vanuzzo D, Gómez de la Cámara A, Gómez Gerique JA, Simons L, McCallum J, Friedlander Y, Fowkes FG, Lee AJ, Taylor J, Guralnik JM, Wallace R, Guralnik J, Blazer DG, Khaw KT, Brenner H, Raum E, Müller H, Rothenbacher D, Jansson JH, Wennberg P, Nissinen A, Donfrancesco C, Salomaa V, Harald K, Jousilahti P, Vartiainen E, Woodward M, D'Agostino RB, Vasan RS, Pencina MJ, Bladbjerg EM, Jørgensen T, Møller L, Jespersen J, Dankner R, Chetrit A, Lubin F, Rosengren A, Lappas G, Björkelund C, Lissner L, Bengtsson C, Cremer P, Nagel D, Tilvis RS, Strandberg TE, Kiyohara Y, Arima H, Doi Y, Ninomiya T, Rodriguez B, Dekker JM, Nijpels G, Stehouwer CD, Rimm E, Pai JK, Sato S, Iso H, Kitamura A, Noda H, Salonen JT, Tuomainen TP, Deeg DJ, Poppelaars JL, Meade TW, Cooper JA, Hedblad B, Berglund G, Engstrom G, Verschuren WM, Blokstra A, Shea S, Döring A, Koenig W, Meisinger C, Mraz W, Bas Bueno de Mesquita H, Kuller LH, Grandits G, Selmer R, Tverdal A, Nystad W, Gillum R, Mussolino M, Hankinson S, Manson JE, Knottenbelt C, Bauer KA, Naito Y, Holme I, Nakagawa H, Miura K, Ducimetiere P, Jouven X, Crespo CJ, Garcia MR, Amouyel P, Arveiler D, Evans A, Ferrieres J, Schulte H, Assmann G, Shepherd J, Packard CJ, Sattar N, Ford I, Cantin B, Després JP, Dagenais GR, Barrett Connor E, Wingard DL, Bettencourt R, Gudnason V, Aspelund T, Sigurdsson G, Thorsson B, Trevisan M, Witteman J, Kardys I, Breteler M, Hofman A, Tunstall Pedoe H, Tavendale R, Lowe GD, Ben Shlomo Y, Davey Smith G, Howard BV, Zhang Y, Umans J, Onat A, Wilsgaard T, Ingelsson E, Lind L, Giedraitis V, Lannfelt L, Gaziano JM, Ridker P, Ulmer H, Diem G, Concin H, Tosetto A, Rodeghiero F, Wassertheil Smoller S, Marmot M, Clarke R, Collins R, Brunner E, Shipley M, Buring J, Cobbe SM, Robertson M, He Y, Marín Ibañez A, Feskens EJ, Kromhout D, Di Angelantonio E, Erqou S, Lewington S, Orfei L, Pennells L, Ray KK, Sarwar N, Alexander M, Thompson A, Walker M, Watson S, Wensley F, Perry P, Danesh J., PANICO, SALVATORE, Hompson, S, Kaptoge, S, White, I, Wood, A, Thompson, Sg, White, Ir, Wood, Am, Perry, Pl, Danesh, J, Tipping, Rw, Ford, Ce, Simpson, Lm, Walldius, G, Jungner, I, Chambless, Le, Panagiotakos, Db, Pitsavos, C, Chrysohoou, C, Stefanadis, C, Knuiman, M, Goldbourt, U, Benderly, M, Tanne, D, Whincup, Ph, Wannamethee, Sg, Morris, Rw, Willeit, J, Kiechl, S, Santer, P, Mayr, A, Lawlor, Da, Yarnell, Jw, Gallacher, J, Casiglia, E, Tikhonoff, V, Nietert, Pj, Sutherland, Se, Bachman, Dl, Keil, Je, Cushman, M, Tracy, Rp, Tybjærg Hansen, A, Nordestgaard, Bg, Benn, M, Frikke Schmidt, R, Giampaoli, S, Palmieri, L, Panico, Salvatore, Vanuzzo, D, Gómez de la Cámara, A, Gómez Gerique, Ja, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, Aj, Taylor, J, Guralnik, Jm, Wallace, R, Guralnik, J, Blazer, Dg, Khaw, Kt, Brenner, H, Raum, E, Müller, H, Rothenbacher, D, Jansson, Jh, Wennberg, P, Nissinen, A, Donfrancesco, C, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, Woodward, M, D'Agostino, Rb, Vasan, R, Pencina, Mj, Bladbjerg, Em, Jørgensen, T, Møller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Rosengren, A, Lappas, G, Björkelund, C, Lissner, L, Bengtsson, C, Cremer, P, Nagel, D, Tilvis, R, Strandberg, Te, Kiyohara, Y, Arima, H, Doi, Y, Ninomiya, T, Rodriguez, B, Dekker, Jm, Nijpels, G, Stehouwer, Cd, Rimm, E, Pai, Jk, Sato, S, Iso, H, Kitamura, A, Noda, H, Salonen, Jt, Tuomainen, Tp, Deeg, Dj, Poppelaars, Jl, Meade, Tw, Cooper, Ja, Hedblad, B, Berglund, G, Engstrom, G, Verschuren, Wm, Blokstra, A, Shea, S, Döring, A, Koenig, W, Meisinger, C, Mraz, W, Bas Bueno de Mesquita, H, Kuller, Lh, Grandits, G, Selmer, R, Tverdal, A, Nystad, W, Gillum, R, Mussolino, M, Hankinson, S, Manson, Je, Knottenbelt, C, Bauer, Ka, Naito, Y, Holme, I, Nakagawa, H, Miura, K, Ducimetiere, P, Jouven, X, Crespo, Cj, Garcia, Mr, Amouyel, P, Arveiler, D, Evans, A, Ferrieres, J, Schulte, H, Assmann, G, Shepherd, J, Packard, Cj, Sattar, N, Ford, I, Cantin, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Wingard, Dl, Bettencourt, R, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Witteman, J, Kardys, I, Breteler, M, Hofman, A, Tunstall Pedoe, H, Tavendale, R, Lowe, Gd, Ben Shlomo, Y, Davey Smith, G, Howard, Bv, Zhang, Y, Umans, J, Onat, A, Wilsgaard, T, Ingelsson, E, Lind, L, Giedraitis, V, Lannfelt, L, Gaziano, Jm, Ridker, P, Ulmer, H, Diem, G, Concin, H, Tosetto, A, Rodeghiero, F, Wassertheil Smoller, S, Marmot, M, Clarke, R, Collins, R, Brunner, E, Shipley, M, Buring, J, Cobbe, Sm, Robertson, M, He, Y, Marín Ibañez, A, Feskens, Ej, Kromhout, D, Di Angelantonio, E, Erqou, S, Lewington, S, Orfei, L, Pennells, L, Ray, Kk, Sarwar, N, Alexander, M, Thompson, A, Walker, M, Watson, S, Wensley, F, Perry, P, and Danesh, J.
Published: 2010

13. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality

Author: Emerging Risk Factors Collaboration, Erqou S, Kaptoge S, Perry PL, Di Angelantonio E, Thompson A, White IR, Marcovina SM, Collins R, Thompson SG, Tipping RW, Ford CE, Simpson LM, Walldius G, Jungner I, Folsom AR, Chambless L, Panagiotakos D, Pitsavos C, Chrysohoou C, Stefanadis C, Goldbourt U, Benderly M, Tanne D, Whincup P, Wannamethee SG, Morris RW, Kiechl S, Willeit J, Santer P, Mayr A, Wald N, Ebrahim S, Lawlor D, Yarnell J, Gallacher J, Casiglia E, Tikhonoff V, Nietert PJ, Sutherland SE, Bachman DL, Cushman M, Psaty BM, Tracy R, Tybjaerg Hansen A, Nordestgaard BG, Frikke Schmidt R, Kamstrup PR, Giampaoli S, Palmieri L, Vanuzzo D, Pilotto L, Gómez de la Cámara A, Gómez Gerique JA, Simons L, McCallum J, Friedlander Y, Fowkes FG, Lee A, Smith FB, Taylor J, Guralnik JM, Phillips CL, Wallace RB, Blazer DG, Brenner H, Raum E, Müller H, Rothenbacher D, Jansson JH, Wennberg P, Nissinen A, Donfrancesco C, Salomaa V, Harald K, Jousilahti P, Vartiainen E, Woodward M, D'Agostino RB, Wolf PA, Vasan RS, Pencina MJ, Bladbjerg EM, Jørgensen T, Møller L, Jespersen J, Dankner R, Chetrit A, Lubin F, Rosengren A, Wilhelmsen L, Lappas G, Eriksson H, Björkelund C, Lissner L, Bengtsson C, Cremer P, Nagel D, Tilvis RS, Strandberg TE, Rodriguez B, Dekker J, Nijpels G, Stehouwer CD, Rimm E, Pai JK, Sato S, Iso H, Kitamura A, Noda H, Salonen JT, Nyyssönen K, Tuomainen TP, Deeg DJ, Poppelaars JL, Hedblad B, Berglund G, Engström G, Verschuren WM, Blokstra A, Döring A, Koenig W, Meisinger C, Mraz W, Bueno de Mesquita HB, Kuller LH, Grandits G, Selmer R, Tverdal A, Nystad W, Gillum RF, Mussolino M, Hankinson S, Manson JE, Cooper JA, Bauer KA, Naito Y, Holme I, Nakagawa H, Miura K, Ducimetiere P, Jouven X, Luc G, Crespo CJ, Garcia Palmieri MR, Amouyel P, Arveiler D, Evans A, Ferrieres J, Schulte H, Assmann G, Shepherd J, Packard CJ, Sattar N, Ford I, Cantin B, Lamarche B, Després JP, Dagenais GR, Barrett Connor E, Daniels LB, Laughlin GA, Gudnason V, Aspelund T, Sigurdsson G, Thorsson B, Trevisan M, Witteman J, Kardys I, Breteler MM, Hofman A, Tunstall Pedoe H, Tavendale R, Lowe G, Ben Shlomo Y, Davey Smith G, Howard BV, Zhang Y, Best L, Umans J, Onat A, Njølstad I, Mathiesen EB, Løchen ML, Wilsgaard T, Ingelsson E, Sundström J, Lind L, Lannfelt L, Gaziano JM, Stampfer M, Ridker PM, Ulmer H, Diem G, Concin H, Tosetto A, Rodeghiero F, Marmot M, Clarke R, Fletcher A, Brunner E, Shipley M, Buring J, Cobbe S, Robertson M, He Y, Marin Ibanñez A, Feskens E, Kromhout D, Walker M, Watson S, Lewington S, Orfei L, Pennells L, Ray KK, Sarwar N, Alexander M, Wensley F, Wood AM, Danesh J., PANICO, SALVATORE, Developmental Genetics, EMGO+ - Lifestyle, Overweight and Diabetes, Emerging Risk Factors, Collaboration, Erqou, S, Kaptoge, S, Perry, Pl, Di Angelantonio, E, Thompson, A, White, Ir, Marcovina, Sm, Collins, R, Thompson, Sg, Tipping, Rw, Ford, Ce, Simpson, Lm, Walldius, G, Jungner, I, Folsom, Ar, Chambless, L, Panagiotakos, D, Pitsavos, C, Chrysohoou, C, Stefanadis, C, Goldbourt, U, Benderly, M, Tanne, D, Whincup, P, Wannamethee, Sg, Morris, Rw, Kiechl, S, Willeit, J, Santer, P, Mayr, A, Wald, N, Ebrahim, S, Lawlor, D, Yarnell, J, Gallacher, J, Casiglia, E, Tikhonoff, V, Nietert, Pj, Sutherland, Se, Bachman, Dl, Cushman, M, Psaty, Bm, Tracy, R, Tybjaerg Hansen, A, Nordestgaard, Bg, Frikke Schmidt, R, Kamstrup, Pr, Giampaoli, S, Palmieri, L, Panico, Salvatore, Vanuzzo, D, Pilotto, L, Gómez de la Cámara, A, Gómez Gerique, Ja, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, A, Smith, Fb, Taylor, J, Guralnik, Jm, Phillips, Cl, Wallace, Rb, Blazer, Dg, Brenner, H, Raum, E, Müller, H, Rothenbacher, D, Jansson, Jh, Wennberg, P, Nissinen, A, Donfrancesco, C, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, Woodward, M, D'Agostino, Rb, Wolf, Pa, Vasan, R, Pencina, Mj, Bladbjerg, Em, Jørgensen, T, Møller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Rosengren, A, Wilhelmsen, L, Lappas, G, Eriksson, H, Björkelund, C, Lissner, L, Bengtsson, C, Cremer, P, Nagel, D, Tilvis, R, Strandberg, Te, Rodriguez, B, Dekker, J, Nijpels, G, Stehouwer, Cd, Rimm, E, Pai, Jk, Sato, S, Iso, H, Kitamura, A, Noda, H, Salonen, Jt, Nyyssönen, K, Tuomainen, Tp, Deeg, Dj, Poppelaars, Jl, Hedblad, B, Berglund, G, Engström, G, Verschuren, Wm, Blokstra, A, Döring, A, Koenig, W, Meisinger, C, Mraz, W, Bueno de Mesquita, Hb, Kuller, Lh, Grandits, G, Selmer, R, Tverdal, A, Nystad, W, Gillum, Rf, Mussolino, M, Hankinson, S, Manson, Je, Cooper, Ja, Bauer, Ka, Naito, Y, Holme, I, Nakagawa, H, Miura, K, Ducimetiere, P, Jouven, X, Luc, G, Crespo, Cj, Garcia Palmieri, Mr, Amouyel, P, Arveiler, D, Evans, A, Ferrieres, J, Schulte, H, Assmann, G, Shepherd, J, Packard, Cj, Sattar, N, Ford, I, Cantin, B, Lamarche, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Daniels, Lb, Laughlin, Ga, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Witteman, J, Kardys, I, Breteler, Mm, Hofman, A, Tunstall Pedoe, H, Tavendale, R, Lowe, G, Ben Shlomo, Y, Davey Smith, G, Howard, Bv, Zhang, Y, Best, L, Umans, J, Onat, A, Njølstad, I, Mathiesen, Eb, Løchen, Ml, Wilsgaard, T, Ingelsson, E, Sundström, J, Lind, L, Lannfelt, L, Gaziano, Jm, Stampfer, M, Ridker, Pm, Ulmer, H, Diem, G, Concin, H, Tosetto, A, Rodeghiero, F, Marmot, M, Clarke, R, Fletcher, A, Brunner, E, Shipley, M, Buring, J, Cobbe, S, Robertson, M, He, Y, Marin Ibanñez, A, Feskens, E, Kromhout, D, Walker, M, Watson, S, Lewington, S, Orfei, L, Pennells, L, Ray, Kk, Sarwar, N, Alexander, M, Wensley, F, Wood, Am, and Danesh, J.
Subjects: medicine.medical_specialty, Context (language use), Coronary Disease, Article, Risk Factors, General & Internal Medicine, Internal medicine, Cause of Death, medicine, Humans, Myocardial infarction, Prospective cohort study, Stroke, biology, business.industry, 11 Medical And Health Sciences, General Medicine, Lipoprotein(a), medicine.disease, Surgery, Relative risk, Nested case-control study, biology.protein, business, Cohort study
Abstract: Udgivelsesdato: 2009-Jul-22 CONTEXT: Circulating concentration of lipoprotein(a) (Lp[a]), a large glycoprotein attached to a low-density lipoprotein-like particle, may be associated with risk of coronary heart disease (CHD) and stroke. OBJECTIVE: To assess the relationship of Lp(a) concentration with risk of major vascular and nonvascular outcomes. STUDY SELECTION: Long-term prospective studies that recorded Lp(a) concentration and subsequent major vascular morbidity and/or cause-specific mortality published between January 1970 and March 2009 were identified through electronic searches of MEDLINE and other databases, manual searches of reference lists, and discussion with collaborators. DATA EXTRACTION: Individual records were provided for each of 126,634 participants in 36 prospective studies. During 1.3 million person-years of follow-up, 22,076 first-ever fatal or nonfatal vascular disease outcomes or nonvascular deaths were recorded, including 9336 CHD outcomes, 1903 ischemic strokes, 338 hemorrhagic strokes, 751 unclassified strokes, 1091 other vascular deaths, 8114 nonvascular deaths, and 242 deaths of unknown cause. Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis. Analyses excluded participants with known preexisting CHD or stroke at baseline. DATA SYNTHESIS: Lipoprotein(a) concentration was weakly correlated with several conventional vascular risk factors and it was highly consistent within individuals over several years. Associations of Lp(a) with CHD risk were broadly continuous in shape. In the 24 cohort studies, the rates of CHD in the top and bottom thirds of baseline Lp(a) distributions, respectively, were 5.6 (95% confidence interval [CI], 5.4-5.9) per 1000 person-years and 4.4 (95% CI, 4.2-4.6) per 1000 person-years. The risk ratio for CHD, adjusted for age and sex only, was 1.16 (95% CI, 1.11-1.22) per 3.5-fold higher usual Lp(a) concentration (ie, per 1 SD), and it was 1.13 (95% CI, 1.09-1.18) following further adjustment for lipids and other conventional risk factors. The corresponding adjusted risk ratios were 1.10 (95% CI, 1.02-1.18) for ischemic stroke, 1.01 (95% CI, 0.98-1.05) for the aggregate of nonvascular mortality, 1.00 (95% CI, 0.97-1.04) for cancer deaths, and 1.00 (95% CI, 0.95-1.06) for nonvascular deaths other than cancer. CONCLUSION: Under a wide range of circumstances, there are continuous, independent, and modest associations of Lp(a) concentration with risk of CHD and stroke that appear exclusive to vascular outcomes.
Published: 2009

14. The Emerging Risk Factors Collaboration: analysis of individual data on lipid, inflammatory and other markers in over 1.1 million participants in 104 prospective studies of cardiovascular diseases

Author: Danesh, J, Erqou, S, Walker, M, Thompson, Sg, Tipping, R, Ford, C, Pressel, S, Walldius, G, Jungner, I, Folsom, Ar, Chambless, Le, Knuiman, M, Whincup, Ph, Wannamethee, Sg, Morris, Rw, Willeit, J, Kiechl, S, Santer, P, Mayr, A, Wald, N, Ebrahim, S, Lawlor, Da, Yarnell, Jw, Gallacher, J, Casiglia, Edoardo, Tikhonoff, Valerie, Nietert, Pj, Sutherland, Se, Bachman, Dl, Keil, Je, Cushman, M, Psaty, Bm, Tracy, Rp, Tybjaerg Hansen, A, Nordestgaard, Bg, Frikke Schmidt, R, Giampaoli, S, Palmieri, L, Panico, S, Vanuzzo, D, Pilotto, L, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, Aj, Smith, Fb, Taylor, J, Guralnik, J, Phillips, C, Wallace, R, Blazer, D, Khaw, Kt, Jansson, Jh, Donfrancesco, C, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, Woodward, M, D'Agostino, Rb, Wolf, Pa, Vasan, Rs, Pencina, Mj, Bladbjerg, Em, Jorgensen, T, Moller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Rosengren, A, Wilhelmsen, L, Lappas, G, Eriksson, H, Bjorkelund, C, Cremer, P, Nagel, D, Tilvis, R, Strandberg, T, Rodriguez, B, Bouter, Lm, Heine, Rj, Dekker, Jm, Nijpels, G, Stehouwer, Cd, Rimm, E, Pai, J, Sato, S, Iso, H, Kitamura, A, Noda, H, Goldbourt, U, Salonen, Jt, Nyyssönen, K, Tuomainen, Tp, Deeg, D, Poppelaars, Jl, Meade, T, Cooper, J, Hedblad, B, Berglund, G, Engstrom, G, Döring, A, Koenig, W, Meisinger, C, Mraz, W, Kuller, L, Selmer, R, Tverdal, A, Nystad, W, Gillum, R, Mussolino, M, Hankinson, S, Manson, J, De Stavola, B, Knottenbelt, C, Cooper, Ja, Bauer, Ka, Rosenberg, Rd, Naito, Y, Holme, I, Nakagawa, H, Miura, H, Ducimetiere, P, Jouven, X, Crespo, C, Garcia Palmieri, M, Amouyel, P, Arveiler, D, Evans, A, Ferrieres, J, Schulte, H, Assmann, G, Shepherd, J, Packard, C, Sattar, N, Cantin, B, Lamarche, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Wingard, D, Bettencourt, R, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Witteman, J, Kardys, I, Breteler, M, Hofman, A, Tunstall Pedoe, H, Tavendale, R, Lowe, Gd, Ben Shlomo, Y, Howard, Bv, Zhang, Y, Best, L, Umans, J, Onat, A, Meade, Tw, Njolstad, I, Mathiesen, E, Lochen, Ml, Wilsgaard, T, Gaziano, Jm, Stampfer, M, Ridker, P, Ulmer, H, Diem, G, Concin, H, Rodeghiero, F, Tosetto, A, Brunner, E, Shipley, M, Buring, J, Cobbe, Sm, Ford, I, Robertson, M, He, Y, Ibanez, Am, Feskens, Ej, Kromhout, D, Collins, R, Di Angelantonio, E, Kaptoge, S, Lewington, S, Orfei, L, Pennells, L, Perry, P, Ray, K, Sarwar, N, Scherman, M, Thompson, A, Watson, S, Wensley, F, White, Ir, Wood, Am, Emerging Risk Factors Collaboration, Interne Geneeskunde, RS: NUTRIM School of Nutrition and Translational Research in Metabolism, RS: CARIM School for Cardiovascular Diseases, Movement Behavior, Executive board Vrije Universiteit, Clinical Child and Family Studies, Sociology and Social Gerontology, Earth and Climate, Environmental Policy Analysis, Developmental Genetics, Danesh, J, Erqou, S, Walker, M, Thompson, Sg, Tipping, R, Ford, C, Pressel, S, Walldius, G, Jungner, I, Folsom, Ar, Chambless, Le, Knuiman, M, Whincup, Ph, Wannamethee, Sg, Morris, Rw, Willeit, J, Kiechl, S, Santer, P, Mayr, A, Wald, N, Ebrahim, S, Lawlor, Da, Yarnell, Jw, Gallacher, J, Casiglia, E, Tikhonoff, V, Nietert, Pj, Sutherland, Se, Bachman, Dl, Keil, Je, Cushman, M, Psaty, Bm, Tracy, Rp, Tybjaerg Hansen, A, Nordestgaard, Bg, Frikke Schmidt, R, Giampaoli, S, Palmieri, L, Panico, Salvatore, Vanuzzo, D, Pilotto, L, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, Aj, Smith, Fb, Taylor, J, Guralnik, J, Phillips, C, Wallace, R, Blazer, D, Khaw, Kt, Jansson, Jh, Donfrancesco, C, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, Woodward, M, D'Agostino, Rb, Wolf, Pa, Vasan, R, Pencina, Mj, Bladbjerg, Em, Jorgensen, T, Moller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Rosengren, A, Wilhelmsen, L, Lappas, G, Eriksson, H, Bjorkelund, C, Cremer, P, Nagel, D, Tilvis, R, Strandberg, T, Rodriguez, B, Bouter, Lm, Heine, Rj, Dekker, Jm, Nijpels, G, Stehouwer, Cd, Rimm, E, Pai, J, Sato, S, Iso, H, Kitamura, A, Noda, H, Goldbourt, U, Salonen, Jt, Nyyssönen, K, Tuomainen, Tp, Deeg, D, Poppelaars, Jl, Meade, T, Cooper, J, Hedblad, B, Berglund, G, Engstrom, G, Döring, A, Koenig, W, Meisinger, C, Mraz, W, Kuller, L, Selmer, R, Tverdal, A, Nystad, W, Gillum, R, Mussolino, M, Hankinson, S, Manson, J, De Stavola, B, Knottenbelt, C, Cooper, Ja, Bauer, Ka, Rosenberg, Rd, Naito, Y, Holme, I, Nakagawa, H, Miura, H, Ducimetiere, P, Jouven, X, Crespo, C, Garcia Palmieri, M, Amouyel, P, Arveiler, D, Evans, A, Ferrieres, J, Schulte, H, Assmann, G, Shepherd, J, Packard, C, Sattar, N, Cantin, B, Lamarche, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Wingard, D, Bettencourt, R, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Witteman, J, Kardys, I, Breteler, M, Hofman, A, Tunstall Pedoe, H, Tavendale, R, Lowe, Gd, Ben Shlomo, Y, Howard, Bv, Zhang, Y, Best, L, Umans, J, Onat, A, Meade, Tw, Njolstad, I, Mathiesen, E, Lochen, Ml, Wilsgaard, T, Gaziano, Jm, Stampfer, M, Ridker, P, Ulmer, H, Diem, G, Concin, H, Rodeghiero, F, Tosetto, A, Brunner, E, Shipley, M, Buring, J, Cobbe, Sm, Ford, I, Robertson, M, He, Y, Ibanez, Am, Feskens, Ej, Kromhout, D, Collins, R, Di Angelantonio, E, Kaptoge, S, Lewington, S, Orfei, L, Pennells, L, Perry, P, Ray, K, Sarwar, N, Scherman, M, Thompson, A, Watson, S, Wensley, F, White, Ir, and Wood, A. M.
Subjects: Databases, Factual, Nutrition and Disease, Epidemiology, Inflammatory markers, middle-aged men, Disease, Leukocyte Count, c-reactive protein, Risk Factors, Voeding en Ziekte, adult-treatment-panel, Prospective Studies, Myocardial infarction, Prospective cohort study, education.field_of_study, biology, plasma-fibrinogen, Asia, Eastern, Confounding, density-lipoprotein cholesterol, Cardiovascular disease, Lipids, myocardial-infarction, Coronary heart disease, Cardiovascular Diseases, Meta-analysis, Lipoproteins, HDL, high blood cholesterol, medicine.medical_specialty, low-dose aspirin, Population, 10-year follow-up, SDG 3 - Good Health and Well-being, Albumins, medicine, Humans, education, Triglycerides, VLAG, Inflammation, Estimation, business.industry, C-reactive protein, medicine.disease, Surgery, Emergency medicine, biology.protein, business, coronary-heart-disease, Biomarkers
Abstract: Many long-term prospective studies have reported on associations of cardiovascular diseases with circulating lipid markers and/or inflammatory markers. Studies have not, however, generally been designed to provide reliable estimates under different circumstances and to correct for within-person variability. The Emerging Risk Factors Collaboration has established a central database on over 1.1 million participants from 104 prospective population-based studies, in which subsets have information on lipid and inflammatory markers, other characteristics, as well as major cardiovascular morbidity and cause-specific mortality. Information on repeat measurements on relevant characteristics has been collected in approximately 340,000 participants to enable estimation of and correction for within-person variability. Re-analysis of individual data will yield up to approximately 69,000 incident fatal or nonfatal first ever major cardiovascular outcomes recorded during about 11.7 million person years at risk. The primary analyses will involve age-specific regression models in people without known baseline cardiovascular disease in relation to fatal or nonfatal first ever coronary heart disease outcomes. This initiative will characterize more precisely and in greater detail than has previously been possible the shape and strength of the age-and sex-specific associations of several lipid and inflammatory markers with incident coronary heart disease outcomes (and, secondarily,with other incident cardiovascular outcomes) under a wide range of circumstances. It will, therefore, help to determine to what extent such associations are independent from possible confounding factors and to what extent such markers (separately and in combination) provide incremental predictive value.
Published: 2007

15. Low-frequency and rare exome chip variants associate with fasting glucose and type 2 diabetes susceptibility

Author: Wessel, J, Chu, AY, Willems, SM, Wang, S, Yaghootkar, H, Brody, JA, Dauriz, M, Hivert, MF, Raghavan, S, Lipovich, L, Hidalgo, B, Fox, K, Huffman, JE, An, P, Lu, YC, Rasmussen-Torvik, LJ, Grarup, N, Ehm, MG, Li, Li, Baldridge, AS, Stancakova, A, Abrol, R, Besse, CL, Boland, A, Bork-Jensen, J, Fornage, M, Freitag, DF, Garcia, ME, Guo, XQ, Hara, K, Isaacs, Aaron, Jakobsdottir, J, Lange, LA, Layton, JC, Li, M, Zhao, JH, Meidtner, K, Morrison, AC, Nalls, MA, Peters, Marjolein, Sabater-Lleal, M, Schurmann, C, Silveira, A, Smith, AV, Southam, L, Stoiber, MH, Strawbridge, RJ, Taylor, KD, Varga, TV, Allin, KH, Amin, Najaf, Aponte, JL, Aung, T, Barbieri, C, Bihlmeyer, NA, Boehnke, M, Bombieri, C, Bowden, DW, Burns, SM, Chen, YN, Chen, YD, Cheng, CY (Ching-Yu), Correa, A, Czajkowski, J, Dehghan, Abbas, Ehret, GB, Eiriksdottir, G, Escher, SA, Farmaki, AE, Franberg, M, Gambaro, G, Giulianini, F, Goddard, WA, Goel, A, Gottesman, O, Grove, ML, Gustafsson, S, Hai, Y, Hallmans, G, Heo, J, Hoffmann, P, Ikram, MK, Jensen, RA, Jorgensen, ME, Jorgensen, T, Karaleftheri, M, Khor, CC, Kirkpatrick, A, Kraja, AT, Kuusisto, J, Lange, Edmee, Lee, IT, Lee, WJ, Leong, A, Liao, JM, Liu, CY, Liu, YM, Lindgren, CM, Linneberg, A, Malerba, G, Mamakou, V, Marouli, E, Maruthur, NM, Matchan, A, McKean-Cowdin, R, McLeod, O, Metcalf, GA, Mohlke, KL, Muzny, DM, Ntalla, I, Palmer, ND, Pasko, D, Peter, A, Rayner, NW, Renstrom, F, Rice, K, Sala, CF, Sennblad, B, Serafetinidis, I, Smith, JA, Soranzo, N, Speliotes, EK, Stahl, EA, Stirrups, K, Tentolouris, N, Thanopoulou, A, Torres, M, Traglia, M, Tsafantakis, E, Javad, S, Yanek, LR, Zengini, E, Becker, DM, Bis, JC, Brown, JB, Cupples, LA, Hansen, T, Ingelsson, E, Karter, AJ, Lorenzo, C, Mathias, RA, Norris, JM, Peloso, GM, Sheu, WHH, Toniolo, D, Vaidya, D, Varma, R, Wagenknecht, LE, Boeing, H, Bottinger, EP, Dedoussis, G, Deloukas, P, Ferrannini, E, Franco Duran, OH, Franks, PW, Gibbs, RA, Gudnason, V, Hamsten, A, Harris, TB, Hattersley, AT, Hayward, C, Hofman, Bert, Jansson, JH, Langenberg, C, Launer, LJ (Lenore), Levy, D, Oostra, Ben, O'Donnell, CJ, O'Rahilly, S, Padmanabhan, S, Pankow, JS, Polasek, O, Province, MA, Rich, SS, Ridker, PM, Rudan, I, Schulze, MB, Smith, BH, Uitterlinden, André, Walker, M, Watkins, H, Wong, TY (Tien Yin), Zeggini, E, Laakso, M, Borecki, IB, Chasman, DI, Pedersen, O, Psaty, BM, Tai, ES, Duijn, Cornelia, Wareham, NJ, Waterworth, DM, Boerwinkle, E, Kao, WHL, Florez, JC, Loos, RJF, Wilson, JG, Frayling, TM, Siscovick, DS, Dupuis, J, Rotter, JI, Meigs, JB, Scott, RA, Goodarzi, MO, Sharp, SJ, Forouhi, NG, Kerrison, ND, Lucarelli, DM, Sims, M, Barroso, I, McCarthy, MI, Arriola, L, Balkau, B, Barricarte, A, Gonzalez, C, Grioni, S, Kaaks, R, Key, TJ, Navarro, C, Nilsson, PM, Overvad, K, Palli, D, Panico, S, Quiros, JR, Rolandsson, O, Sacerdote, C, Sanchez, MJ (Maria-Jose), Slimani, N, Tjonneland, A, Tumino, R, van der A, DL, van der Schouw, YT, Riboli, E, Wessel, J, Chu, AY, Willems, SM, Wang, S, Yaghootkar, H, Brody, JA, Dauriz, M, Hivert, MF, Raghavan, S, Lipovich, L, Hidalgo, B, Fox, K, Huffman, JE, An, P, Lu, YC, Rasmussen-Torvik, LJ, Grarup, N, Ehm, MG, Li, Li, Baldridge, AS, Stancakova, A, Abrol, R, Besse, CL, Boland, A, Bork-Jensen, J, Fornage, M, Freitag, DF, Garcia, ME, Guo, XQ, Hara, K, Isaacs, Aaron, Jakobsdottir, J, Lange, LA, Layton, JC, Li, M, Zhao, JH, Meidtner, K, Morrison, AC, Nalls, MA, Peters, Marjolein, Sabater-Lleal, M, Schurmann, C, Silveira, A, Smith, AV, Southam, L, Stoiber, MH, Strawbridge, RJ, Taylor, KD, Varga, TV, Allin, KH, Amin, Najaf, Aponte, JL, Aung, T, Barbieri, C, Bihlmeyer, NA, Boehnke, M, Bombieri, C, Bowden, DW, Burns, SM, Chen, YN, Chen, YD, Cheng, CY (Ching-Yu), Correa, A, Czajkowski, J, Dehghan, Abbas, Ehret, GB, Eiriksdottir, G, Escher, SA, Farmaki, AE, Franberg, M, Gambaro, G, Giulianini, F, Goddard, WA, Goel, A, Gottesman, O, Grove, ML, Gustafsson, S, Hai, Y, Hallmans, G, Heo, J, Hoffmann, P, Ikram, MK, Jensen, RA, Jorgensen, ME, Jorgensen, T, Karaleftheri, M, Khor, CC, Kirkpatrick, A, Kraja, AT, Kuusisto, J, Lange, Edmee, Lee, IT, Lee, WJ, Leong, A, Liao, JM, Liu, CY, Liu, YM, Lindgren, CM, Linneberg, A, Malerba, G, Mamakou, V, Marouli, E, Maruthur, NM, Matchan, A, McKean-Cowdin, R, McLeod, O, Metcalf, GA, Mohlke, KL, Muzny, DM, Ntalla, I, Palmer, ND, Pasko, D, Peter, A, Rayner, NW, Renstrom, F, Rice, K, Sala, CF, Sennblad, B, Serafetinidis, I, Smith, JA, Soranzo, N, Speliotes, EK, Stahl, EA, Stirrups, K, Tentolouris, N, Thanopoulou, A, Torres, M, Traglia, M, Tsafantakis, E, Javad, S, Yanek, LR, Zengini, E, Becker, DM, Bis, JC, Brown, JB, Cupples, LA, Hansen, T, Ingelsson, E, Karter, AJ, Lorenzo, C, Mathias, RA, Norris, JM, Peloso, GM, Sheu, WHH, Toniolo, D, Vaidya, D, Varma, R, Wagenknecht, LE, Boeing, H, Bottinger, EP, Dedoussis, G, Deloukas, P, Ferrannini, E, Franco Duran, OH, Franks, PW, Gibbs, RA, Gudnason, V, Hamsten, A, Harris, TB, Hattersley, AT, Hayward, C, Hofman, Bert, Jansson, JH, Langenberg, C, Launer, LJ (Lenore), Levy, D, Oostra, Ben, O'Donnell, CJ, O'Rahilly, S, Padmanabhan, S, Pankow, JS, Polasek, O, Province, MA, Rich, SS, Ridker, PM, Rudan, I, Schulze, MB, Smith, BH, Uitterlinden, André, Walker, M, Watkins, H, Wong, TY (Tien Yin), Zeggini, E, Laakso, M, Borecki, IB, Chasman, DI, Pedersen, O, Psaty, BM, Tai, ES, Duijn, Cornelia, Wareham, NJ, Waterworth, DM, Boerwinkle, E, Kao, WHL, Florez, JC, Loos, RJF, Wilson, JG, Frayling, TM, Siscovick, DS, Dupuis, J, Rotter, JI, Meigs, JB, Scott, RA, Goodarzi, MO, Sharp, SJ, Forouhi, NG, Kerrison, ND, Lucarelli, DM, Sims, M, Barroso, I, McCarthy, MI, Arriola, L, Balkau, B, Barricarte, A, Gonzalez, C, Grioni, S, Kaaks, R, Key, TJ, Navarro, C, Nilsson, PM, Overvad, K, Palli, D, Panico, S, Quiros, JR, Rolandsson, O, Sacerdote, C, Sanchez, MJ (Maria-Jose), Slimani, N, Tjonneland, A, Tumino, R, van der A, DL, van der Schouw, YT, and Riboli, E
Abstract: Fasting glucose and insulin are intermediate traits for type 2 diabetes. Here we explore the role of coding variation on these traits by analysis of variants on the HumanExome BeadChip in 60,564 non-diabetic individuals and in 16,491 T2D cases and 81,877 controls. We identify a novel association of a low-frequency nonsynonymous SNV in GLP1R (A316T; rs10305492; MAF = 1.4%) with lower FG (beta = -0.09 +/- 0.01 mmol l(-1), P = 3.4 x 10(-12)), T2D risk (OR[95% CI] = 0.86[0.76-0.96], P = 0.010), early insulin secretion (beta = -0.07 +/- 0.035 pmol(insulin) mmol(glucose)(-1), P = 0.048), but higher 2-h glucose (beta = 0.16 +/- 0.05 mmol l(-1), P = 4.3 x 10(-4)). We identify a gene-based association with FG at G6PC2 (p(SKAT) = 6.8 x 10(-6)) driven by four rare protein-coding SNVs (H177Y, Y207S, R283X and S324P). We identify rs651007 (MAF = 20%) in the first intron of ABO at the putative promoter of an antisense lncRNA, associating with higher FG (beta = 0.02 +/- 0.004 mmol l(-1), P = 1.3 x 10(-8)). Our approach identifies novel coding variant associations and extends the allelic spectrum of variation underlying diabetes-related quantitative traits and T2D susceptibility.
Published: 2015

16. Bayesian methods for meta-analysis of causal relationships estimated using genetic instrumental variables

Author: Burgess, S, Thompson, SG, Andrews, G, Samani, NJ, Hall, A, Whincup, P, Morris, R, Lawlor, DA, Davey Smith, G, Timpson, N, Ebrahim, S, Ben-Shlomo, Y, Brown, M, Ricketts, S, Sandhu, M, Reiner, A, Psaty, B, Lange, L, Cushman, M, Hung, J, Thompson, P, Beilby, J, Warrington, N, Palmer, LJ, Nordestgaard, BG, Tybjaerg-Hansen, A, Zacho, J, Wu, C, Lowe, G, Tzoulaki, I, Kumari, M, Yamamoto, JF, Chiodini, B, Franzosi, M, Hankey, GJ, Jamrozik, K, Palmer, L, Rimm, E, Pai, J, Heckbert, S, Bis, J, Anand, S, Engert, J, Collins, R, Clarke, R, Melander, O, Berglund, G, Ladenvall, P, Johansson, L, Jansson, JH, Hallmans, G, Hingorani, A, Humphries, S, Manson, J, Watkins, H, Hopewell, J, Saleheen, D, Frossard, R, Danesh, J, Sattar, N, Robertson, M, Shepherd, J, Schaefer, E, Hofman, A, Witteman, JC, Kardys, I, de Faire, U, Bennet, A, Ford, I, Packard, C, Casas, JP, Smeeth, L, Wensley, F, Bowden, J, Di Angelantonio, E, Gao, P, Shah, T, Verzilli, C, Walker, M, and Whittaker, J
Subjects: Genetic Markers, Statistics and Probability, Epidemiology, Bayesian probability, Context (language use), Bayes Theorem, Biostatistics, Polymorphism, Single Nucleotide, Article, Hierarchical database model, Bayes' theorem, Meta-Analysis as Topic, Statistics, Mendelian randomization, Econometrics, Humans, Models, Statistical, Instrumental variable, C-Reactive Protein/genetics/metabolism, Fibrinogen, Regression, Fibrinogen/metabolism, C-Reactive Protein, Phenotype, Meta-analysis
Abstract: Genetic markers can be used as instrumental variables, in an analogous way to randomization in a clinical trial, to estimate the causal relationship between a phenotype and an outcome variable. Our purpose is to extend the existing methods for such Mendelian randomization studies to the context of multiple genetic markers measured in multiple studies, based on the analysis of individual participant data. First, for a single genetic marker in one study, we show that the usual ratio of coefficients approach can be reformulated as a regression with heterogeneous error in the explanatory variable. This can be implemented using a Bayesian approach, which is next extended to include multiple genetic markers. We then propose a hierarchical model for undertaking a meta-analysis of multiple studies, in which it is not necessary that the same genetic markers are measured in each study. This provides an overall estimate of the causal relationship between the phenotype and the outcome, and an assessment of its heterogeneity across studies. As an example, we estimate the causal relationship of blood concentrations of C-reactive protein on fibrinogen levels using data from 11 studies. These methods provide a flexible framework for efficient estimation of causal relationships derived from multiple studies. Issues discussed include weak instrument bias, analysis of binary outcome data such as disease risk, missing genetic data, and the use of haplotypes. Stat Med
Published: 2010

17. Adult height and the risk of cause-specific death and vascular morbidity in 1 million people : individual participant meta-analysis

Author: Wormser, David, Di Angelantonio, Emanuele, Kaptoge, Stephen, Wood, Angela M., Gao, Pei, Sun, Qi, Walldius, Goeran, Selmer, Randi, Verschuren, W. M. Monique, Bueno-de-Mesquita, H. Bas, Engstrom, Gunnar, Ridker, Paul M., Njolstad, Inger, Iso, Hiroyasu, Holme, Ingar, Giampaoli, Simona, Tunstall-Pedoe, Hugh, Gaziano, J. Michael, Brunner, Eric, Kee, Frank, Tosetto, Alberto, Meisinger, Christa, Brenner, Hermann, Ducimetiere, Pierre, Whincup, Peter H., Tipping, Robert W., Ford, Ian, Cremer, Peter, Hofman, Albert, Wilhelmsen, Lars, Clarke, Robert, de Boer, Ian H., Jukema, J. Wouter, Ibanez, Alejandro Marin, Lawlor, Debbie A., D'Agostino, Ralph B., Sr., Rodriguez, Beatriz, Casiglia, Edoardo, Stehouwer, Coen D. A., Simons, Leon A., Nietert, Paul J., Barrett-Connor, Elizabeth, Panagiotakos, Demosthenes B., Bjorkelund, Cecilia, Strandberg, Timo E., Wassertheil-Smoller, Sylvia, Blazer, Dan G., Meade, Tom W., Welin, Lennart, Svärdsudd, Kurt, Woodward, Mark, Nissinen, Aulikki, Kromhout, Daan, Jorgensen, Torben, Tilvis, Reijo S., Guralnik, Jack M., Rosengren, Annika, Taylor, James O., Kiechl, Stefan, Dagenais, Gilles R., Fowkes, F. Gerry R., Wallace, Robert B., Khaw, Kay-Tee, Shaffer, Jonathan A., Visser, Marjolein, Kauhanen, Jussi, Salonen, Jukka T., Gallacher, John, Ben-Shlomo, Yoav, Kitamura, Akihiko, Sundström, Johan, Wennberg, Patrik, Kiyohara, Yutaka, Daimon, Makoto, Gomez de la Camara, Agustin, Cooper, Jackie A., Onat, Altan, Devereux, Richard, Mukamal, Kenneth J., Dankner, Rachel, Knuiman, Matthew W., Crespo, Carlos J., Gansevoort, Ron T., Goldbourt, Uri, Nordestgaard, Borge G., Shaw, Jonathan E., Mussolino, Michael, Nakagawa, Hidaeki, Fletcher, Astrid, Kuller, Lewis H., Gillum, Richard F., Gudnason, Vilmundur, Assmann, Gerd, Wald, Nicholas, Jousilahti, Pekka R., Greenland, Philip, Trevisan, Maurizio, Ulmer, Hanno, Butterworth, Adam S., Folsom, Aaron R., Davey-Smith, George, Hu, Frank B., Danesh, John, Tipping, Ford, CE, Simpson, Walldius, G, Jungner, I, Folsom, AR, Demerath, Franceschini, N, Lutsey, Panagiotakos, DB, Pitsavos, C, Chrysohoou, C, Stefanadis, Shaw, JE, Atkins, R, Zimmet, PZ, Barr, EL, Knuiman, MW, Whincup, Wannamethee, Morris, Willeit, J, Kiechl, Weger, Oberhollenzer, F, Wald, N, Ebrahim, S, Lawlor, DA, Gallacher, J, Ben-Shlomo, Yarnell, Casiglia, Tikhonoff, Greenland, P, Shay, Garside, Nietert, Sutherland, SE, Bachman, DL, Keil, de Boer, IH, Kizer, JR, Psaty, BM, Mukamal, KJ, Nordestgaard, BG, Tybjærg-Hansen A, A, Jensen, GB, Schnohr, P, Giampaoli, S, Palmieri, Panico, Pilotto, L, Vanuzzo, D, de la Cámara, AG, Simons, LA, Simons, J, McCallum, J, Friedlander, Gerry, F, Fowkes, R, Price, JF, Lee, AJ, Taylor, Taylor JO, Guralnik, JM, Phillips, CL, Kohout, FJ, Cornoni-Huntley, JC, Blazer, DG, Guralnik, Khaw, KT, Wareham, NJ, Brenner, H, Schöttker, B, Müller, H, Rothenbacher, D, Wennberg, P, Jansson, JH, Nissinen, A, Donfrancesco, C, Woodward, M, Vartiainen, E, Jousilahti, PR, Harald, K, Salomaa, V, D'Agostino, RB, Vasan, RS, Fox, CS, Pencina, MJ, Daimon, M, Oizumi, T, Kayama, T, Kato, T, Bladbjerg, EM, Danesh, J, Wormser, David, Di Angelantonio, Emanuele, Kaptoge, Stephen, Wood, Angela M., Gao, Pei, Sun, Qi, Walldius, Goeran, Selmer, Randi, Verschuren, W. M. Monique, Bueno-de-Mesquita, H. Bas, Engstrom, Gunnar, Ridker, Paul M., Njolstad, Inger, Iso, Hiroyasu, Holme, Ingar, Giampaoli, Simona, Tunstall-Pedoe, Hugh, Gaziano, J. Michael, Brunner, Eric, Kee, Frank, Tosetto, Alberto, Meisinger, Christa, Brenner, Hermann, Ducimetiere, Pierre, Whincup, Peter H., Tipping, Robert W., Ford, Ian, Cremer, Peter, Hofman, Albert, Wilhelmsen, Lars, Clarke, Robert, de Boer, Ian H., Jukema, J. Wouter, Ibanez, Alejandro Marin, Lawlor, Debbie A., D'Agostino, Ralph B., Sr., Rodriguez, Beatriz, Casiglia, Edoardo, Stehouwer, Coen D. A., Simons, Leon A., Nietert, Paul J., Barrett-Connor, Elizabeth, Panagiotakos, Demosthenes B., Bjorkelund, Cecilia, Strandberg, Timo E., Wassertheil-Smoller, Sylvia, Blazer, Dan G., Meade, Tom W., Welin, Lennart, Svärdsudd, Kurt, Woodward, Mark, Nissinen, Aulikki, Kromhout, Daan, Jorgensen, Torben, Tilvis, Reijo S., Guralnik, Jack M., Rosengren, Annika, Taylor, James O., Kiechl, Stefan, Dagenais, Gilles R., Fowkes, F. Gerry R., Wallace, Robert B., Khaw, Kay-Tee, Shaffer, Jonathan A., Visser, Marjolein, Kauhanen, Jussi, Salonen, Jukka T., Gallacher, John, Ben-Shlomo, Yoav, Kitamura, Akihiko, Sundström, Johan, Wennberg, Patrik, Kiyohara, Yutaka, Daimon, Makoto, Gomez de la Camara, Agustin, Cooper, Jackie A., Onat, Altan, Devereux, Richard, Mukamal, Kenneth J., Dankner, Rachel, Knuiman, Matthew W., Crespo, Carlos J., Gansevoort, Ron T., Goldbourt, Uri, Nordestgaard, Borge G., Shaw, Jonathan E., Mussolino, Michael, Nakagawa, Hidaeki, Fletcher, Astrid, Kuller, Lewis H., Gillum, Richard F., Gudnason, Vilmundur, Assmann, Gerd, Wald, Nicholas, Jousilahti, Pekka R., Greenland, Philip, Trevisan, Maurizio, Ulmer, Hanno, Butterworth, Adam S., Folsom, Aaron R., Davey-Smith, George, Hu, Frank B., Danesh, John, Tipping, Ford, CE, Simpson, Walldius, G, Jungner, I, Folsom, AR, Demerath, Franceschini, N, Lutsey, Panagiotakos, DB, Pitsavos, C, Chrysohoou, C, Stefanadis, Shaw, JE, Atkins, R, Zimmet, PZ, Barr, EL, Knuiman, MW, Whincup, Wannamethee, Morris, Willeit, J, Kiechl, Weger, Oberhollenzer, F, Wald, N, Ebrahim, S, Lawlor, DA, Gallacher, J, Ben-Shlomo, Yarnell, Casiglia, Tikhonoff, Greenland, P, Shay, Garside, Nietert, Sutherland, SE, Bachman, DL, Keil, de Boer, IH, Kizer, JR, Psaty, BM, Mukamal, KJ, Nordestgaard, BG, Tybjærg-Hansen A, A, Jensen, GB, Schnohr, P, Giampaoli, S, Palmieri, Panico, Pilotto, L, Vanuzzo, D, de la Cámara, AG, Simons, LA, Simons, J, McCallum, J, Friedlander, Gerry, F, Fowkes, R, Price, JF, Lee, AJ, Taylor, Taylor JO, Guralnik, JM, Phillips, CL, Kohout, FJ, Cornoni-Huntley, JC, Blazer, DG, Guralnik, Khaw, KT, Wareham, NJ, Brenner, H, Schöttker, B, Müller, H, Rothenbacher, D, Wennberg, P, Jansson, JH, Nissinen, A, Donfrancesco, C, Woodward, M, Vartiainen, E, Jousilahti, PR, Harald, K, Salomaa, V, D'Agostino, RB, Vasan, RS, Fox, CS, Pencina, MJ, Daimon, M, Oizumi, T, Kayama, T, Kato, T, Bladbjerg, EM, and Danesh, J
Abstract: Background The extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain. Methods We calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual-participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies. Results For people born between 1900 and 1960, mean adult height increased 0.5-1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96-0.99) for death from any cause, 0.94 (0.93-0.96) for death from vascular causes, 1.04 (1.03-1.06) for death from cancer and 0.92 (0.90-0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12-1.42) for risk of melanoma death to 0.84 (0.80-0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators. Conclusion Adult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases., Karl Michaëlsson (Department of Surgical Sciences, Orthopaedics, Uppsala University, Sweden) contributed to this study.
Published: 2012
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18. Estimated intake of milk fat is negatively associated with cardiovascular risk factors and does not increase the risk of a first acute myocardial infarction. A prospective case-control study

Author: Warensjö, Eva, Jansson, JH, Berglund, Lars, Boman, K, Ahren, B, Weinehall, L, Lindahl, B, Hallmans, G, Vessby, Bengt, Warensjö, Eva, Jansson, JH, Berglund, Lars, Boman, K, Ahren, B, Weinehall, L, Lindahl, B, Hallmans, G, and Vessby, Bengt
Abstract: Milk fat is high in saturated fatty acids (SFA) and high intakes of SFA are associated with cardiovascular diseases. The aim of the present study was to prospectively evaluate the potential risk of a first-ever acute myocardial infarction (AMI) in relation to the estimated milk-fat intake, reflected as the proportions of pentadecanoic acid (15 : 0) and heptadecanoic acid (17 : 0) in serum lipid esters. This was evaluated in a study population selected within the Västerbotten Intervention Program and the northern Sweden 'Monitoring of Trends and Determinants in Cardiovascular disease' survey populations. A prospective case-control design was used. The proportions of the biomarkers were lower in the cases (n 78) than in the controls (n 156), who were matched for age, sex, sampling time and geographical region. The standardised odds ratios of becoming an AMI case were between 0.7 and 0.8 for the biomarkers. The proportions of 15 : 0 and 17 : 0 in serum phospholipids were significantly and negatively correlated to serum concentrations of plasminogen activator inhibitor-1, tissue-type plasminogen activator, triacylglycerols, insulin, specific insulin, pro-insulin and leptin (all P<0.0001), suggesting a negative relationship to the insulin-resistance syndrome and the risk of CHD. Adjustment for BMI did not materially change the relationships. Although there seems to be a negative association between milk-fat intake as mirrored by the proportions of 15 : 0 and 17 : 0 in serum lipid esters and a first-ever AMI, adjustment for clinical risk factors removed this relationship.
Published: 2004
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19. Cardiovascular disease and diabetes in the Northern Sweden Health and Disease Study Cohort : evaluation of risk factors and their interactions.

Author: Hallmans, Göran, Agren, A, Johansson, G, Johansson, Anders, Stegmayr, Birgitta, Jansson, JH, Lindahl, B, Rolandsson, Olov, Söderberg, Stefan, Nilsson, M, Johansson, Ingegerd, Weinehall, Lars, Hallmans, Göran, Agren, A, Johansson, G, Johansson, Anders, Stegmayr, Birgitta, Jansson, JH, Lindahl, B, Rolandsson, Olov, Söderberg, Stefan, Nilsson, M, Johansson, Ingegerd, and Weinehall, Lars
Abstract: The purpose of this paper is, first, to describe the organization, sampling procedures, availability of samples/database, ethical considerations, and quality control program of the Northern Sweden Health and Disease Study Cohort. Secondly, some examples are given of studies on cardiovascular disease and diabetes with a focus on the biomarker programme. The cohort has been positioned as a national and international resource for scientific research.
Published: 2003
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20. Markers of high fish intake are associated with decreased risk of a firstmyocardial infarction.

Author: Hallgren, CG, Hallmans, G, Jansson, JH, Marklund, SL, Huhtasaari, F, Schutz, A, Stromberg, U, Vessby, B, Skerfving, S, Hallgren, CG, Hallmans, G, Jansson, JH, Marklund, SL, Huhtasaari, F, Schutz, A, Stromberg, U, Vessby, B, and Skerfving, S
Published: 2001

21. Homozygosity for the C677-->T mutation of 5,10-methylenetetrahydrofolate reductase and total plasma homocyst(e) ine are not associated with greater than normal risk of a first myocardial infarction in northern Sweden

Author: Thøgersen, AM, Nilsson, TK, Dahlén, G., Jansson, JH, Boman, K., Huhtasaari, F., Hallmans, G., Thøgersen, AM, Nilsson, TK, Dahlén, G., Jansson, JH, Boman, K., Huhtasaari, F., and Hallmans, G.
Abstract: BACKGROUND: Results of several case-control studies have shown elevated total plasma homocyst(e)ine (TPH) and homozygosity for the point mutation C677-->T in the gene for 5,10-methylenetetrahydrofolate reductase (MTHFR) to be associated with a greater than normal risk of atherosclerotic vascular disease. However, there have been few epidemiologic studies and the interpretation of the results is not clear-cut. OBJECTIVE: To elucidate whether homozygosity for the point mutation C677-->T in the gene for MTHFR, and TPH are risk factors for a first myocardial infarction. DESIGN: A prospective nested case-control study in Northern Sweden. METHODS: Among more than 36000 persons screened, 78 cases satisfied the inclusion criterion of having developed, after sampling, a first myocardial infarction. For each case, two controls matched for sex and age were randomly selected. RESULTS: We found no statistically significant difference among the prevalences of the three possible MTHFR genotypes -/- (no mutation), +/+ (both alleles have the mutation), and +/- among cases and controls in univariate conditional logistic regression analysis. Mean levels of TPH in patients and controls were 12.2+/-4.9 and 12.2+/-3.5 micromol/l (means +/- SD), respectively (NS). CONCLUSIONS: In this study neither homozygosity for the point mutation C677-->T in the gene for MTHFR nor TPH was related to a greater than normal risk of a first myocardial infarction for members of the population of northern Sweden. Further research is needed in order to show whether TPH is an independent risk factor for a first myocardial infarction.
Published: 2001

22. High plasminogen activator inhibitor and tissue plasminogen activator levels in plasma precede a first acute myocardial infarction in both men and women. : Evidence for the fibrinolytic system as an independent primary risk factor

Author: Thøgersen, AM, Jansson, JH, Boman, K., Nilsson, TK, Weinehall, L., Huhtasaari, F., Hallmans, G., Thøgersen, AM, Jansson, JH, Boman, K., Nilsson, TK, Weinehall, L., Huhtasaari, F., and Hallmans, G.
Abstract: BACKGROUND: In patients with established ischemic heart disease, prospective cohort studies have indicated that plasminogen activator inhibitor (PAI-1), the inhibitor of the fibrinolytic system, may predict cardiovascular events. So far, there have been no primary prospective studies of PAI-1. METHODS AND RESULTS: The aim of the present study was to test whether plasma levels of PAI-1, tissue-type plasminogen activator (tPA), von Willebrand factor (vWF), and thrombomodulin (TM) could predict the occurrence of a first acute myocardial infarction (AMI) in a population with high prevalence of coronary heart disease by use of a prospective nested case-control design. Mass concentrations of PAI-1 and tPA were significantly higher for the 78 subjects who developed a first AMI compared with the 156 references matched for age, sex, and sampling time; for tPA, this increase was independent of smoking habits, body mass index, hypertension, diabetes, cholesterol, and apolipoprotein A-I. The ratio of quartile 4 to 1 for tPA was 5.9 for a patient to develop a first AMI. The association between tPA and AMI was seen in both men and women. Increased levels of vWF were associated with AMI in a univariate analysis. High levels of TM were associated with AMI in women but not in men. CONCLUSIONS: The plasma levels of PAI-1, tPA, and vWF are associated with subsequent development of a first AMI; for PAI-1 and tPA, this relation was found in both men and women. For tPA but not for PAI-1 and vWF, this association is independent of established risk factors.
Published: 1998

23. Efficacy and safety of anticoagulant prophylaxis to prevent venous thromboembolism in acutely ill medical inpatients: a meta-analysis.

Author: Själander A, Jansson JH, Bergqvist D, Eriksson H, Carlberg B, and Svensson P
Abstract: OBJECTIVES: Venous thromboembolism (VTE) is a potentially serious complication of hospitalization and immobilization. The use of anticoagulant prophylaxis in acutely ill medical inpatients is still under debate. New data including a recent meta-analysis have recently been published. We aim at studying the efficacy and safety of anticoagulant prophylaxis in acutely ill medical inpatients, and demonstrate differences between meta-analyses due to different data extraction from the heterogeneous studies included. SUBJECTS: The Cochrane Library, MEDLINE and EMBASE were searched from 1980 to present. Manual searches were performed regarding abstracts from major meetings. Seven blinded randomized controlled clinical trials assessing the prophylactic effect of heparin in acutely ill medical patients were identified and included in the meta-analysis. RESULTS: Low-molecular weight heparin (LMWH) prophylaxis prevented 48% of symptomatic pulmonary embolism (PE), 48% of symptomatic deep vein thrombosis (DVT) (not significant) and 51% of asymptomatic DVT. A nonsignificant trend towards higher bleeding risk during LMWH prophylaxis was found. Death was not significantly affected. We compared our data with a recent meta-analysis with different study selection and data extraction and found similar results. CONCLUSIONS: As DVT and PE are manifestations of the same illness, VTE, one can argue that anticoagulant prophylaxis prevents approximately half of the expected events. Most medical inpatients have short hospital stays, and a low risk of VTE. The important task for the clinician is to identify patients with a sufficiently high risk of symptomatic VTE to warrant LMWH prophylaxis. Despite differences in study selection and data extraction, our study shows results similar to a recent meta-analysis. [ABSTRACT FROM AUTHOR]
Published: 2008
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24. Fish intake, mercury, long-chain n-3 polyunsaturated fatty acids and risk of stroke in northern Sweden.

Author: Wennberg M, Bergdahl IA, Stegmayr B, Hallmans G, Lundh T, Skerfving S, Strömberg U, Vessby B, and Jansson JH
Published: 2007
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25. Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies

Author: Triglyceride Coronary Disease Genetics Consortium, Emerging Risk Factors Collaboration, Sarwar, N, Sandhu, Ms, Ricketts, Sl, Butterworth, As, Di Angelantonio, E, Boekholdt, Sm, Ouwehand, W, Watkins, H, Samani, Nj, Saleheen, D, Lawlor, D, Reilly, Mp, Hingorani, Ad, Talmud, Pj, Collaborators: Braund PS, Danesh J., Hall, As, Thompson, J, März, W, Sivapalaratnam, S, Soranzo, N, Trip, M, Lawlor, Da, Casas, Jp, Ebrahim, S, Arsenault, Bj, Khaw, Kt, Wareham, Nj, Grallert, H, Illig, T, Humphries, Se, Talmud, T, Rader, Dj, He, J, Clarke, R, Hamsten, A, Hopewell, Jc, Frossard, P, Deloukas, P, Danesh, J, Ye, S, Simpson, Ia, Onat, A, Kömürcü Bayrak, E, Martinelli, Nicola, Olivieri, Oliviero, Girelli, Domenico, Kivimäki, M, Kumari, M, Aouizerat, Be, Baum, L, Campos, H, Chaaba, R, Chen, Bs, Cho, Ey, Evans, D, Hill, J, Hsu, La, Hubacek, Ja, Lai, Cq, Lee, Jh, Klos, K, Liu, H, Masana, L, Melegh, B, Nabika, T, Ribalta, J, Ruiz Narvaez, E, Thomas, Gn, Tomlinson, B, Szalai, C, Vaverkova, H, Yamada, Y, Yang, Y, Tipping, Rw, Ford, Ce, Pressel, Sl, Ballantyne, C, Brautbar, A, Knuiman, M, Whincup, Ph, Wannamethee, Sg, Morris, Rw, Kiechl, S, Willeit, J, Santer, P, Mayr, A, Wald, N, Yarnell, Jw, Gallacher, J, Casiglia, E, Tikhonoff, V, Cushman, M, Psaty, Bm, Tracy, Rp, Tybjaerg Hansen, A, Nordestgaard, Bg, Benn, M, Frikke Schmidt, R, Giampaoli, S, Palmieri, L, Panico, S, Vanuzzo, D, Pilotto, L, de la Cámara AG, Gómez Gerique JA, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, Aj, Taylor, J, Guralnik, Jm, Phillips, Cl, Wallace, R, Blazer, Dg, Brenner, H, Raum, E, Müller, H, Rothenbacher, D, Jansson, Jh, Wennberg, P, Nissinen, A, Donfrancesco, C, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, D'Agostino, Rb, Vasan, Rs, Pencina, Mj, Bladbjerg, Em, Jørgensen, T, Møller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Björkelund, C, Lissner, L, Bengtsson, C, Cremer, P, Nagel, D, Rodriguez, B, Dekker, Jm, Nijpels, G, Stehouwer, Cd, Sato, S, Iso, H, Kitamura, A, Noda, H, Salonen, Jt, Nyyssönen, K, Tuomainen, Tp, Voutilainen, S, Meade, Tw, Cooper, Ja, Kuller, Lh, Grandits, G, Gillum, R, Mussolino, M, Rimm, E, Hankinson, S, Manson, Ja, Pai, Jk, Bauer, Ka, Naito, Y, Amouyel, P, Arveiler, D, Evans, A, Ferrières, J, Schulte, H, Assmann, G, Packard, Cj, Sattar, N, Westendorp, Rg, Buckley, Bm, Cantin, B, Lamarche, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Wingard, Dl, Bettencourt, R, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Tunstall Pedoe, H, Tavendale, R, Lowe, Gd, Woodward, M, Howard, Bv, Zhang, Y, Best, L, Umans, J, Ben Shlomo, Y, Davey Smith, G, Njølstad, I, Mathiesen, Eb, Løchen, Ml, Wilsgaard, T, Ingelsson, E, Lind, L, Giedraitis, V, Michaëlsson, K, Brunner, E, Shipley, M, Ridker, P, Buring, J, Shepherd, J, Cobbe, Sm, Ford, I, Robertson, M, Ibañez, Am, Feskens, Ej, Kromhout, D, Walker, M, Watson, S, Collins, R, Kaptoge, S, Perry, Pl, Thompson, A, Thompson, Sg, White, Ir, Wood, Am, Danesh, J., ACS - Amsterdam Cardiovascular Sciences, Cardiology, Vascular Medicine, Interne Geneeskunde, MUMC+: MA Interne Geneeskunde (3), RS: CARIM School for Cardiovascular Diseases, Sarwar, N, Sandhu, M, Ricketts, Sl, Butterworth, A, Braund, P, Hall, A, Samani, Nj, Thompson, J, März, W, Ouwehand, W, Sivapalaratnam, S, Soranzo, N, Trip, M, Lawlor, Da, Casas, Jp, Ebrahim, S, Arsenault, Bj, Boekholdt, Sm, Khaw, Kt, Wareham, Nj, Grallert, H, Illig, T, Humphries, Se, Talmud, T, Rader, Dj, He, J, Reilly, Mp, Clarke, R, Hamsten, A, Hopewell, Jc, Watkins, H, Saleheen, D, Frossard, P, Deloukas, P, Danesh, J, Ye, S, Simpson, Ia, Onat, A, Kömürcü Bayrak, E, Martinelli, N, Olivieri, O, Girelli, D, Hingorani, Ad, Kivimäki, M, Kumari, M, Aouizerat, Be, Baum, L, Campos, H, Chaaba, R, Chen, B, Cho, Ey, Evans, D, Hill, J, Hsu, La, Hubacek, Ja, Lai, Cq, Lee, Jh, Klos, K, Liu, H, Masana, L, Melegh, B, Nabika, T, Ribalta, J, Ruiz Narvaez, E, Thomas, Gn, Tomlinson, B, Szalai, C, Vaverkova, H, Yamada, Y, Yang, Y, Kastelein, Jj, Tipping, Rw, Ford, Ce, Pressel, Sl, Ballantyne, C, Brautbar, A, Knuiman, M, Whincup, Ph, Wannamethee, Sg, Morris, Rw, Kiechl, S, Willeit, J, Santer, P, Mayr, A, Wald, N, Yarnell, Jw, Gallacher, J, Casiglia, E, Tikhonoff, V, Cushman, M, Psaty, Bm, Tracy, Rp, Tybjaerg Hansen, A, Nordestgaard, Bg, Benn, M, Frikke Schmidt, R, Giampaoli, S, Palmieri, L, Panico, Salvatore, Vanuzzo, D, Pilotto, L, de la Cámara, Ag, Gómez Gerique, Ja, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, Aj, Taylor, J, Guralnik, Jm, Phillips, Cl, Wallace, R, Blazer, Dg, Brenner, H, Raum, E, Müller, H, Rothenbacher, D, Jansson, Jh, Wennberg, P, Nissinen, A, Donfrancesco, C, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, D'Agostino, Rb, Vasan, R, Pencina, Mj, Bladbjerg, Em, Jørgensen, T, Møller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Björkelund, C, Lissner, L, Bengtsson, C, Cremer, P, Nagel, D, Rodriguez, B, Dekker, Jm, Nijpels, G, Stehouwer, Cd, Sato, S, Iso, H, Kitamura, A, Noda, H, Salonen, Jt, Nyyssönen, K, Tuomainen, Tp, Voutilainen, S, Meade, Tw, Cooper, Ja, Kuller, Lh, Grandits, G, Gillum, R, Mussolino, M, Rimm, E, Hankinson, S, Manson, Ja, Pai, Jk, Bauer, Ka, Naito, Y, Amouyel, P, Arveiler, D, Evans, A, Ferrières, J, Schulte, H, Assmann, G, Packard, Cj, Sattar, N, Westendorp, Rg, Buckley, Bm, Cantin, B, Lamarche, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Wingard, Dl, Bettencourt, R, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Tunstall Pedoe, H, Tavendale, R, Lowe, Gd, Woodward, M, Howard, Bv, Zhang, Y, Best, L, Umans, J, Ben Shlomo, Y, Davey Smith, G, Njølstad, I, Mathiesen, Eb, Løchen, Ml, Wilsgaard, T, Ingelsson, E, Lind, L, Giedraitis, V, Michaëlsson, K, Brunner, E, Shipley, M, Ridker, P, Buring, J, Shepherd, J, Cobbe, Sm, Ford, I, Robertson, M, Ibañez, Am, Feskens, Ej, Kromhout, D, Walker, M, Watson, S, Collins, R, Di Angelantonio, E, Kaptoge, S, Perry, Pl, Thompson, A, Thompson, Sg, White, Ir, Wood, Am, Lawlor, D, Talmud, Pj, Danesh, J., Epidemiology and Data Science, General practice, and EMGO - Lifestyle, overweight and diabetes
Subjects: Very low-density lipoprotein, Nutrition and Disease, Heart disease, Coronary Disease, Lipoproteins, VLDL, 030204 cardiovascular system & hematology, low-density-lipoprotein apolipoprotein-a-v transfer protein heart-disease myocardial-infarction metabolic syndrome rich lipoproteins risk dyslipidemia association, Bioinformatics, chemistry.chemical_compound, 0302 clinical medicine, triglyceride, APOA5 gene polymorphysm, coronary heart disease, Gene Frequency, Risk Factors, Voeding en Ziekte, Medicine, Myocardial infarction, Promoter Regions, Genetic, risk, 0303 health sciences, Men, Mendelian Randomization Analysis, Articles, General Medicine, Lipids, myocardial-infarction, 3. Good health, Lipoproteins, LDL, Low-density lipoprotein, Lipoproteins, HDL, apolipoprotein-a-v, Receptor, medicine.medical_specialty, Genotype, transfer protein, Snp, Polymorphism, Single Nucleotide, metabolic syndrome, 03 medical and health sciences, Internal medicine, Humans, Particle Size, Apolipoproteins A, Triglycerides, VLAG, 030304 developmental biology, low-density-lipoprotein, Triglyceride, business.industry, dyslipidemia, association, rich lipoproteins, medicine.disease, heart-disease, Apolipoproteins, Endocrinology, chemistry, Apolipoprotein A-V, Metabolic syndrome, business, Dyslipidemia
Abstract: Udgivelsesdato: May-8 BACKGROUND: Whether triglyceride-mediated pathways are causally relevant to coronary heart disease is uncertain. We studied a genetic variant that regulates triglyceride concentration to help judge likelihood of causality. METHODS: We assessed the -1131T>C (rs662799) promoter polymorphism of the apolipoprotein A5 (APOA5) gene in relation to triglyceride concentration, several other risk factors, and risk of coronary heart disease. We compared disease risk for genetically-raised triglyceride concentration (20,842 patients with coronary heart disease, 35,206 controls) with that recorded for equivalent differences in circulating triglyceride concentration in prospective studies (302 430 participants with no history of cardiovascular disease; 12,785 incident cases of coronary heart disease during 2.79 million person-years at risk). We analysed -1131T>C in 1795 people without a history of cardiovascular disease who had information about lipoprotein concentration and diameter obtained by nuclear magnetic resonance spectroscopy. FINDINGS: The minor allele frequency of -1131T>C was 8% (95% CI 7-9). -1131T>C was not significantly associated with several non-lipid risk factors or LDL cholesterol, and it was modestly associated with lower HDL cholesterol (mean difference per C allele 3.5% [95% CI 2.6-4.6]; 0.053 mmol/L [0.039-0.068]), lower apolipoprotein AI (1.3% [0.3-2.3]; 0.023 g/L [0.005-0.041]), and higher apolipoprotein B (3.2% [1.3-5.1]; 0.027 g/L [0.011-0.043]). By contrast, for every C allele inherited, mean triglyceride concentration was 16.0% (95% CI 12.9-18.7), or 0.25 mmol/L (0.20-0.29), higher (p=4.4x10(-24)). The odds ratio for coronary heart disease was 1.18 (95% CI 1.11-1.26; p=2.6x10(-7)) per C allele, which was concordant with the hazard ratio of 1.10 (95% CI 1.08-1.12) per 16% higher triglyceride concentration recorded in prospective studies. -1131T>C was significantly associated with higher VLDL particle concentration (mean difference per C allele 12.2 nmol/L [95% CI 7.7-16.7]; p=9.3x10(-8)) and smaller HDL particle size (0.14 nm [0.08-0.20]; p=7.0x10(-5)), factors that could mediate the effects of triglyceride. INTERPRETATION: These data are consistent with a causal association between triglyceride-mediated pathways and coronary heart disease. FUNDING: British Heart Foundation, UK Medical Research Council, Novartis.
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26. Increased levels of tissue plasminogen activator antigen in essential hypertension. A population-based study in Sweden.

Author: Eliasson M, Jansson JH, Nilsson P, Asplund K, Eliasson, M, Jansson, J H, Nilsson, P, and Asplund, K
Published: 1997
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27. Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies

Author: Emerging Risk Factors Collaboration, Sarwar N, Gao P, Seshasai SR, Gobin R, Kaptoge S, Di Angelantonio E, Ingelsson E, Lawlor DA, Selvin E, Stampfer M, Stehouwer CD, Lewington S, Pennells L, Thompson A, Sattar N, White IR, Ray KK, Danesh J. Tipping RW, Ford CE, Pressel SL, Folsom AR, Chambless LE, Wagenknecht LE, Panagiotakos DB, Pitsavos C, Chrysohoou C, Stefanadis C, Knuiman M, Whincup PH, Wannamethee SG, Morris RW, Kiechl S, Willeit J, Oberhollenzer F, Mayr A, Wald N, Ebrahim S, Yarnell JW, Gallacher J, Casiglia E, Tikhonoff V, Nietert PJ, Sutherland SE, Bachman DL, Keil JE, de Boer IH, Kizer JR, Mukamal KJ, Tybjaerg Hansen A, Nordestgaard BG, Benn M, Frikke Schmidt R, Palmieri L, Vanuzzo D, Pilotto L, de la Cámara AG, Rubio MA, Simons L, McCallum J, Friedlander Y, Fowkes FG, Lee AJ, Taylor J, Guralnik JM, Phillips CL, Wallace R, Blazer DG, Khaw KT, Brenner H, Raum E, Müller H, Rothenbacher D, Jansson JH, Wennberg P, Nissinen A, Donfrancesco C, Giampaoli S, Salomaa V, Harald K, Jousilahti P, Vartiainen E, Woodward M, D'Agostino RB, Vasan RS, Fox CS, Pencina MJ, Bladbjerg E, Jørgensen T, Møller L, Jespersen J, Dankner R, Chetrit A, Lubin F, Wilhelmsen L, Eriksson H, Svärdsudd K, Welin L, Rosengren A, Lappas G, Björkelund C, Lissner L, Bengtsson C, Cremer P, Nagel D, Strandberg TE, Tilvis RS, Miettinen TA, Kiyohara Y, Arima H, Doi Y, Ninomiya T, Rodriguez B, Dekker JM, Nijpels G, Rimm E, Pai JK, Sato S, Iso H, Kitamura A, Noda H, Goldbourt U, Nyyssönen K, Tuomainen TP, Salonen JT, Deeg D, Poppelaars JL, Meade TW, Cooper JA, Hedblad B, Berglund G, Engström G, Verschuren WM, Blokstra A, Cushman M, Psaty BM, Shea S, Döring A, Koenig W, Meisinger C, Mraz W, Bueno de Mesquita HB, Fletcher A, Kuller LH, Grandits G, Selmer R, Tverdal A, Nystad W, Gillum R, Mussolino M, Hankinson S, Manson JE, Bauer KA, Davidson KW, Kirkland S, Shaffer J, Korin MR, Holme I, Ducimetiere P, Jouven X, Bakker SJ, Gansevoort RT, Hillege HL, Crespo CJ, Garcia Palmieri MR, Amouyel P, Arveiler D, Evans A, Ferrières J, Schulte H, Assmann G, Westendorp RG, Buckley BM, Packard CJ, Cantin B, Lamarche B, Després JP, Dagenais GR, Barrett Connor E, Wingard DL, Bettencourt R, Gudnason V, Aspelund T, Sigurdsson G, Thorsson B, Trevisan M, Witteman J, Kardys I, Breteler M, Hofman A, Tunstall Pedoe H, Tavendale R, Lowe GD, Howard BV, Zhang Y, Best L, Umans J, Ben Shlomo Y, Davey Smith G, Onat A, Hergenç G, Can G, Njølstad I, Mathiesen EB, Løchen ML, Wilsgaard T, Zethelius B, Risérus U, Berne C, Gaziano JM, Ridker P, Ulmer H, Diem G, Concin H, Tosetto A, Rodeghiero F, Tinker L, Liu S, Marmot IM, Clarke R, Collins R, Brunner E, Shipley M, Buring J, Shepherd J, Cobbe SM, Ford I, Robertson M, Ibañez AM, Feskens EJ, Kromhout D, Walker M, Watson S, Alexander M, Erqou S, Haycock P, Perry PL, Thompson SG, Wood AM, Wormser D, Danesh J., PANICO, SALVATORE, Interne Geneeskunde, RS: NUTRIM - R1 - Metabolic Syndrome, RS: CARIM School for Cardiovascular Diseases, Emerging Risk Factors, Collaboration, Sarwar, N, Gao, P, Seshasai, Sr, Gobin, R, Kaptoge, S, Di Angelantonio, E, Ingelsson, E, Lawlor, Da, Selvin, E, Stampfer, M, Stehouwer, Cd, Lewington, S, Pennells, L, Thompson, A, Sattar, N, White, Ir, Ray, Kk, Danesh J., Tipping RW, Ford, Ce, Pressel, Sl, Folsom, Ar, Chambless, Le, Wagenknecht, Le, Panagiotakos, Db, Pitsavos, C, Chrysohoou, C, Stefanadis, C, Knuiman, M, Whincup, Ph, Wannamethee, Sg, Morris, Rw, Kiechl, S, Willeit, J, Oberhollenzer, F, Mayr, A, Wald, N, Ebrahim, S, Yarnell, Jw, Gallacher, J, Casiglia, E, Tikhonoff, V, Nietert, Pj, Sutherland, Se, Bachman, Dl, Keil, Je, de Boer, Ih, Kizer, Jr, Mukamal, Kj, Tybjaerg Hansen, A, Nordestgaard, Bg, Benn, M, Frikke Schmidt, R, Palmieri, L, Panico, Salvatore, Vanuzzo, D, Pilotto, L, de la Cámara, Ag, Rubio, Ma, Simons, L, Mccallum, J, Friedlander, Y, Fowkes, Fg, Lee, Aj, Taylor, J, Guralnik, Jm, Phillips, Cl, Wallace, R, Blazer, Dg, Khaw, Kt, Brenner, H, Raum, E, Müller, H, Rothenbacher, D, Jansson, Jh, Wennberg, P, Nissinen, A, Donfrancesco, C, Giampaoli, S, Salomaa, V, Harald, K, Jousilahti, P, Vartiainen, E, Woodward, M, D'Agostino, Rb, Vasan, R, Fox, C, Pencina, Mj, Bladbjerg, E, Jørgensen, T, Møller, L, Jespersen, J, Dankner, R, Chetrit, A, Lubin, F, Wilhelmsen, L, Eriksson, H, Svärdsudd, K, Welin, L, Rosengren, A, Lappas, G, Björkelund, C, Lissner, L, Bengtsson, C, Cremer, P, Nagel, D, Strandberg, Te, Tilvis, R, Miettinen, Ta, Kiyohara, Y, Arima, H, Doi, Y, Ninomiya, T, Rodriguez, B, Dekker, Jm, Nijpels, G, Rimm, E, Pai, Jk, Sato, S, Iso, H, Kitamura, A, Noda, H, Goldbourt, U, Nyyssönen, K, Tuomainen, Tp, Salonen, Jt, Deeg, D, Poppelaars, Jl, Meade, Tw, Cooper, Ja, Hedblad, B, Berglund, G, Engström, G, Verschuren, Wm, Blokstra, A, Cushman, M, Psaty, Bm, Shea, S, Döring, A, Koenig, W, Meisinger, C, Mraz, W, Bueno de Mesquita, Hb, Fletcher, A, Kuller, Lh, Grandits, G, Selmer, R, Tverdal, A, Nystad, W, Gillum, R, Mussolino, M, Hankinson, S, Manson, Je, Bauer, Ka, Davidson, Kw, Kirkland, S, Shaffer, J, Korin, Mr, Holme, I, Ducimetiere, P, Jouven, X, Bakker, Sj, Gansevoort, Rt, Hillege, Hl, Crespo, Cj, Garcia Palmieri, Mr, Amouyel, P, Arveiler, D, Evans, A, Ferrières, J, Schulte, H, Assmann, G, Westendorp, Rg, Buckley, Bm, Packard, Cj, Cantin, B, Lamarche, B, Després, Jp, Dagenais, Gr, Barrett Connor, E, Wingard, Dl, Bettencourt, R, Gudnason, V, Aspelund, T, Sigurdsson, G, Thorsson, B, Trevisan, M, Witteman, J, Kardys, I, Breteler, M, Hofman, A, Tunstall Pedoe, H, Tavendale, R, Lowe, Gd, Howard, Bv, Zhang, Y, Best, L, Umans, J, Ben Shlomo, Y, Davey Smith, G, Onat, A, Hergenç, G, Can, G, Njølstad, I, Mathiesen, Eb, Løchen, Ml, Wilsgaard, T, Zethelius, B, Risérus, U, Berne, C, Gaziano, Jm, Ridker, P, Ulmer, H, Diem, G, Concin, H, Tosetto, A, Rodeghiero, F, Tinker, L, Liu, S, Marmot, Im, Clarke, R, Collins, R, Brunner, E, Shipley, M, Buring, J, Shepherd, J, Cobbe, Sm, Ford, I, Robertson, M, Ibañez, Am, Feskens, Ej, Kromhout, D, Walker, M, Watson, S, Alexander, M, Erqou, S, Haycock, P, Perry, Pl, Thompson, Sg, Wood, Am, Wormser, D, Danesh, J., and University of Groningen
Subjects: Adult, Blood Glucose, Male, medicine.medical_specialty, PATHOPHYSIOLOGY, 030209 endocrinology & metabolism, Coronary Disease, Disease, 030204 cardiovascular system & hematology, THERAPY, Diabetes Complications, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Diabetes mellitus, Internal medicine, General & Internal Medicine, medicine, Diabetes Mellitus, Humans, CORONARY-HEART-DISEASE, Prospective cohort study, Stroke, Aged, Glucose Metabolism Disorders, business.industry, Vascular disease, MORTALITY, Absolute risk reduction, ASIA-PACIFIC REGION, WOMEN, General Medicine, Fasting, 11 Medical And Health Sciences, Articles, Middle Aged, medicine.disease, Impaired fasting glucose, 3. Good health, Endocrinology, Blood pressure, ATHEROSCLEROSIS, Cardiovascular Diseases, CARDIOVASCULAR-DISEASES, Female, coronary-heart-disease asia-pacific region cardiovascular-diseases task-force pathophysiology atherosclerosis mortality therapy women, business, TASK-FORCE
Abstract: Summary Background Uncertainties persist about the magnitude of associations of diabetes mellitus and fasting glucose concentration with risk of coronary heart disease and major stroke subtypes. We aimed to quantify these associations for a wide range of circumstances. Methods We undertook a meta-analysis of individual records of diabetes, fasting blood glucose concentration, and other risk factors in people without initial vascular disease from studies in the Emerging Risk Factors Collaboration. We combined within-study regressions that were adjusted for age, sex, smoking, systolic blood pressure, and body-mass index to calculate hazard ratios (HRs) for vascular disease. Findings Analyses included data for 698 782 people (52 765 non-fatal or fatal vascular outcomes; 8·49 million person-years at risk) from 102 prospective studies. Adjusted HRs with diabetes were: 2·00 (95% CI 1·83–2·19) for coronary heart disease; 2·27 (1·95–2·65) for ischaemic stroke; 1·56 (1·19–2·05) for haemorrhagic stroke; 1·84 (1·59–2·13) for unclassified stroke; and 1·73 (1·51–1·98) for the aggregate of other vascular deaths. HRs did not change appreciably after further adjustment for lipid, inflammatory, or renal markers. HRs for coronary heart disease were higher in women than in men, at 40–59 years than at 70 years and older, and with fatal than with non-fatal disease. At an adult population-wide prevalence of 10%, diabetes was estimated to account for 11% (10–12%) of vascular deaths. Fasting blood glucose concentration was non-linearly related to vascular risk, with no significant associations between 3·90 mmol/L and 5·59 mmol/L. Compared with fasting blood glucose concentrations of 3·90–5·59 mmol/L, HRs for coronary heart disease were: 1·07 (0·97–1·18) for lower than 3·90 mmol/L; 1·11 (1·04–1·18) for 5·60–6·09 mmol/L; and 1·17 (1·08–1·26) for 6·10–6·99 mmol/L. In people without a history of diabetes, information about fasting blood glucose concentration or impaired fasting glucose status did not significantly improve metrics of vascular disease prediction when added to information about several conventional risk factors. Interpretation Diabetes confers about a two-fold excess risk for a wide range of vascular diseases, independently from other conventional risk factors. In people without diabetes, fasting blood glucose concentration is modestly and non-linearly associated with risk of vascular disease. Funding British Heart Foundation, UK Medical Research Council, and Pfizer.

28. Gender differences in trends of acute myocardial infarction events: the Northern Sweden MONICA study 1985 - 2004.

Author: Lundblad D, Holmgren L, Jansson JH, Näslund U, Eliasson M, Lundblad, Dan, Holmgren, Lars, Jansson, Jan-Håkan, Näslund, Ulf, and Eliasson, Mats
Abstract: Background: The registration of non-fatal and fatal MI events initiated 1985 in the WHO MONICA project has been ongoing in northern Sweden since the end of the WHO project in 1995. The purpose of the present study was to analyze gender differences in first and recurrent events, case fatality and mortality in myocardial infarction (MI) in Northern Sweden during the 20-year period 1985 - 2004.Methods: Diagnosed MI events in subjects aged 25-64 years in the Counties of Norrbotten and Västerbotten were validated according to the MONICA protocol. The total number of events registered up to January 1, 2005 was 11,763: 9,387 in men and 2,376 in women.Results: The proportion of male/female events has decreased from 5.5:1 to 3:1. For males the reductions were 30% and 70% for first and recurrent MI, respectively, and for women 0% and 40% in the 55-64 year group. For both sexes a 50% reduction in 28-day case fatality was seen in the 25-64 year-group. Mortality was reduced by 69% and 45% in men and women, respectively.Conclusion: First and recurrent events of myocardial infarction was markedly reduced in men over the 20-year observation period, but for women the reduction was seen only for recurrent infarctions. Case fatality, on the other hand, was markedly reduced for both sexes. As a result of the positive effects on incidence and case fatality a substantial reduction was seen in total mortality, most pronounced for men. [ABSTRACT FROM AUTHOR]
Published: 2008
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29. Modified Mediterranean diet and survival after myocardial infarction

Author: Y. T. van der Schouw, Philippos Orfanos, B. Van Guelpen, V. Pala, C. A. Gonzalez, Petra H.M. Peeters, Anne Tjønneland, María José Sánchez, Antonia Trichopoulou, Vassiliki Benetou, S Bingham, Timothy J. Key, S. Rohrmann, Theodora Psaltopoulou, Kay-Tee Khaw, Christina Bamia, Kim Overvad, Erik Berg Schmidt, Concha Moreno, Nerea Larrañaga, F. Clavel-Chapelon, J. Linseisen, Salvatore Panico, J. H. Jansson, M. C. Boutron-Ruault, M-D Chirlaque, Teresa Norat, Giovanna Masala, Jytte Halkjær, Cornelia Weikert, H. Boeing, Paolo Boffetta, Dimitrios Trichopoulos, R. Tumino, Carlotta Sacerdote, Marga C. Ocké, Marie-Noël Vercambre, H. B. Bueno-De-Mesquita, Elio Riboli, E. A. Spencer, Trichopoulou, A, Bamia, C, Norat, T, Overvad, K, Schmidt, Eb, Tjonneland, A, Halkjaer, J, CLAVEL CHAPELON, F, Vercambre, Mn, BOUTRON RUAULT, Mc, Linseisen, J, Rohrmann, S, Boeing, H, Weikert, C, Benetou, V, Psaltopoulou, T, Orfanos, P, Boffetta, P, Masala, G, Pala, V, Panico, Salvatore, Tumino, R, Sacerdote, C, BUENO DE MESQUITA, Hb, Ocke, Mc, Peeters, Ph, VAN DER SCHOUW, Yt, Gonzalez, C, Sanchez, Mj, Chirlaque, Md, Moreno, C, Larranaga, N, VAN GUELPEN, B, Jansson, Jh, Bingham, S, Khaw, Kt, Spencer, Ea, Key, T, Riboli, E, Trichopoulos, D., Trichopoulou, A., Bamia, C., Norat, T., Overvad, K., Schmidt, E.B., Tjønneland, A., Halkjær, J., Clavel-Chapelon, F., Vercambre, M.-N., Boutron-Ruault, M.-C., Linseisen, J., Rohrmann, S., Boeing, H., Weikert, C., Benetou, V., Psaltopoulou, T., Orfanos, P., Boffetta, P., Masala, G., Pala, V., Panico, S., Tumino, R., Sacerdote, C., Bueno-De-Mesquita, H.B., Ocke, M.C., Peeters, P.H., Van Der Schouw, Y.T., González, C., Sanchez, M.J., Chirlaque, M.D., Moreno, C., Larrañaga, N., Van Guelpen, B., Jansson, J.-H., Bingham, S., Khaw, K.-T., Spencer, E.A., Key, T., Riboli, E., and University of Groningen
Subjects: Male, COUNTRIES, medicine.medical_specialty, Mediterranean diet, Epidemiology, ALCOHOL, Diet, Mediterranean, survival, elderly, Modified Mediterranean diet survival myocardial infarction EPIC-Elderly study, Food group, PEOPLE, medicine, Humans, CORONARY-HEART-DISEASE, COHORT, Prospective Studies, Myocardial infarction, ddc:610, Survival rate, Aged, Proportional Hazards Models, RISK, business.industry, Proportional hazards model, Mortality rate, MORTALITY, Middle Aged, Nutrition Surveys, medicine.disease, CANCER, European Prospective Investigation into Cancer and Nutrition, Surgery, Europe, Survival Rate, Standardized mortality ratio, myocardial infarction, Female, NUTRITION, business, FOLLOW-UP, Demography
Abstract: Mediterranean diet is associated with lower incidence of coronary heart disease, and two randomised trials indicated that it improves prognosis of coronary patients. These trials, however, relied on a total of 100 deaths and evaluated designer diets in the clinical context. We have evaluated the association of adherence to the modified Mediterranean diet, in which unsaturates were substituted for monounsaturates, with survival among elderly with previous myocardial infarction within the European Prospective Investigation into Cancer and nutrition (EPIC) study. As of December 2003, after a median follow-up of 6.7 years, 2671 EPIC participants from nine countries were 60 years or older and had prevalent myocardial infarction but no stroke or cancer at enrolment, complete information on dietary intakes and important covariates and known survival status. Adherence to the modified Mediterranean diet was assessed through a 10-unit-scale. Mortality ratio in relation to modified Mediterranean diet was estimated through Cox regression controlling for possible confounding. Increased adherence to modified Mediterranean diet by two units was associated with 18% lower overall mortality rate (95% confidence interval 7-27%, fixed effects model). There was no significant heterogeneity by sex, age at enrolment, or country, although the association tended to be less evident among northern Europeans. Associations between food groups contributing to the modified Mediterranean diet and mortality were generally weak. A diet inspired by the Mediterranean pattern that can be easily adopted by Western populations is associated with substantial reduction of total mortality of coronary patients in the community. © 2007 Springer Science+Business Media B.V.
Published: 2007

30. Dietary fibre intake and ischaemic heart disease mortality: the European Prospective Investigation into Cancer and Nutrition-Heart study

Author: Bo Hedblad, Y. T. van der Schouw, Rikke Egeberg, Rudolf Kaaks, Conchi Moreno-Iribas, Timothy J. Key, J. R. Quirós, Pamela Ferrari, M-J Sanchez, S-C Chuang, Sabina Sieri, H. B. Bueno-de-Mesquita, José María Huerta, Anne Tjønneland, V Ouranos, Miren Dorronsoro, Francesca L. Crowe, Teresa Norat, J.M.A. Boer, Elio Riboli, Heiner Boeing, Elisavet Valanou, Giuseppe Matullo, Genevieve Buckland, Nicholas J. Wareham, K-T Khaw, Joline W.J. Beulens, Kim Overvad, Giovanna Masala, B Teucher, A-K Illner, Salvatore Panico, John Danesh, Erik Berg Schmidt, Rosario Tumino, P N Appleby, J. H. Jansson, Patrik Wennberg, Antonia Trichopoulou, Cornelia Weikert, Crowe, Fl, Key, Tj, Appleby, Pn, Overvad, K, Schmidt, Eb, Egeberg, R, Tj?nneland, A, Kaaks, R, Teucher, B, Boeing, H, Weikert, C, Trichopoulou, A, Ouranos, V, Valanou, E, Masala, G, Sieri, S, Panico, Salvatore, Tumino, R, Matullo, G, Bueno de Mesquita, Hb, Boer, Jm, Beulens, Jw, van der Schouw, Yt, Quir?s, Jr, Buckland, G, S?nchez, Mj, Dorronsoro, M, Huerta, Jm, Moreno Iribas, C, Hedblad, B, Jansson, Jh, Wennberg, P, Khaw, Kt, Wareham, N, Ferrari, P, Illner, Ak, Chuang, Sc, Norat, T, Danesh, J, Riboli, E., Epidemiology and Data Science, ACS - Diabetes & metabolism, ACS - Heart failure & arrhythmias, and APH - Health Behaviors & Chronic Diseases
Subjects: Dietary Fiber, Male, medicine.medical_specialty, Myocardial Ischemia, Medicine (miscellaneous), Nutritional Status, Disease, prospective cohort studies, Lower risk, Body Mass Index, ischaemic heart disease, Risk Factors, Internal medicine, Neoplasms, Surveys and Questionnaires, Vegetables, medicine, Humans, cardiovascular diseases, Prospective Studies, Prospective cohort study, Life Style, Nutrition and Dietetics, business.industry, dietary fibre, Dietary fibre, Middle Aged, Confidence interval, European Prospective Investigation into Cancer and Nutrition, Surgery, Diet, Europe, Relative risk, Fruit, Regression Analysis, Female, business, Edible Grain, Body mass index, Follow-Up Studies
Abstract: Background/objectives:Evidence from prospective studies is consistent in showing an inverse association between dietary fibre intake and risk of ischaemic heart disease (IHD), but whether dietary fibre from various food sources differ in their effect on IHD risk is less clear. The objective of this study was to assess the associations of total and food sources of dietary fibre with IHD mortality in the European Prospective Investigation into Cancer and Nutrition-Heart study.Subjects/methods:Participants were 306 331 men and women from eight European countries. Dietary fibre intake was assessed using centre or country-specific diet questionnaires and calibrated using a 24-h diet recall.Results:After an average follow-up of 11.5 years, there were 2381 IHD deaths among participants without cardiovascular disease at baseline. The calibrated intake of dietary fibre was inversely related with IHD mortality; each 10 g/day was associated with a 15% lower risk (relative risk (RR) 0.85; 95% confidence interval (CI): 0.73-0.99, P=0.031). There was no difference in the associations of the individual food sources of dietary fibre with the risk of IHD mortality; RR for each 5 g/day higher cereal fibre intake was 0.91 (CI: 0.82-1.01), RR for each 2.5 g/day fruit fibre intake was 0.94 (CI: 0.88-1.01) and RR for each 2.5 g/day vegetable fibre intake was 0.90 (95% CI: 0.76-1.07).Conclusion:A higher consumption of dietary fibre is associated with a lower risk of fatal IHD with no clear difference in the association with IHD for fibre from cereals, fruits or vegetables.European Journal of Clinical Nutrition advance online publication, 23 May 2012; doi:10.1038/ejcn.2012.51.
Published: 2012

31. Leukotriene A4 Hydrolase and Hepatocyte Growth Factor Are Risk Factors of Sudden Cardiac Death Due to First-Ever Myocardial Infarction.

Author: Landfors F, Vikström S, Wennberg P, Jansson JH, Andersson J, and Chorell E
Subjects: Case-Control Studies, Cholesterol, Death, Sudden, Cardiac etiology, Epoxide Hydrolases, Glucose, Humans, Inflammation complications, Prospective Studies, Risk Factors, Hepatocyte Growth Factor, Myocardial Infarction complications
Abstract: Patients at a high risk for sudden cardiac death (SCD) without previous history of cardiovascular disease remain a challenge to identify. Atherosclerosis and prothrombotic states involve inflammation and non-cardiac tissue damage that may play active roles in SCD development. Therefore, we hypothesized that circulating proteins implicated in inflammation and tissue damage are linked to the future risk of SCD. We conducted a prospective nested case-control study of SCD cases with verified myocardial infarction (N = 224) and matched controls without myocardial infarction (N = 224), aged 60 ± 10 years time and median time to event was 8 years. Protein concentrations (N = 122) were measured using a proximity extension immunoassay. The analyses revealed 14 proteins significantly associated with an increased risk of SCD, from which two remained significant after adjusting for smoking status, systolic blood pressure, BMI, cholesterol, and glucose levels. We identified leukotriene A4 hydrolase (LTA4H, odds ratio 1.80, corrected confidence interval (CI corr ) 1.02-3.17) and hepatocyte growth factor (HGF; odds ratio 1.81, CI corr 1.06-3.11) as independent risk markers of SCD. Elevated LTA4H may reflect increased systemic and pulmonary neutrophilic inflammatory processes that can contribute to atherosclerotic plaque instability. Increased HGF levels are linked to obesity-related metabolic disturbances that are more prevalent in SCD cases than the controls.
Published: 2022
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32. Swedish snus use is associated with mortality: a pooled analysis of eight prospective studies.

Author: Byhamre ML, Araghi M, Alfredsson L, Bellocco R, Engström G, Eriksson M, Galanti MR, Jansson JH, Lager A, Lundberg M, Östergren PO, Pedersen NL, Trolle Lagerros Y, Ye W, Wennberg P, and Magnusson C
Subjects: Humans, Male, Proportional Hazards Models, Prospective Studies, Sweden epidemiology, Tobacco Use epidemiology, Tobacco, Smokeless adverse effects
Abstract: Background: The health consequences of the use of Swedish snus, including its relationship with mortality, have not been fully established. We investigated the relationship between snus use and all-cause and cause-specific mortality (death due to cardiovascular diseases, cancer diseases and all other reasons, respectively) in a nationwide collaborative pooling project., Methods: We followed 169 103 never-smoking men from eight Swedish cohort studies, recruited in 1978-2010. Shared frailty models with random effects at the study level were used in order to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) of mortality associated with snus use., Results: Exclusive current snus users had an increased risk of all-cause mortality (aHR 1.28, 95% CI 1.20-1.35), cardiovascular mortality (aHR 1.27, 95% CI 1.15-1.41) and other cause mortality (aHR 1.37, 95% CI 1.24-1.52) compared with never-users of tobacco. The risk of cancer mortality was also increased (aHR 1.12, 95% CI 1.00-1.26). These mortality risks increased with duration of snus use, but not with weekly amount., Conclusions: Snus use among men is associated with increased all-cause mortality, cardiovascular mortality, with death from other causes and possibly with increased cancer mortality., (© The Author(s) 2020. Published by Oxford University Press on behalf of the International Epidemiological Association.)
Published: 2021
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33. Lysophospholipids as Predictive Markers of ST-Elevation Myocardial Infarction (STEMI) and Non-ST-Elevation Myocardial Infarction (NSTEMI).

Author: Chorell E, Olsson T, Jansson JH, and Wennberg P
Abstract: The present study explored patterns of circulating metabolites and proteins that can predict future risk for ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI). We conducted a prospective nested case-control study in northern Sweden in individuals who developed STEMI (N = 50) and NSTEMI (N = 50) within 5 years and individually matched controls (N = 100). Fasted plasma samples were subjected to multiplatform mass spectrometry-based metabolomics and multiplex protein analyses. Multivariate analyses were used to elucidate infarction-specific metabolite and protein risk profiles associated with future incident STEMI and NSTEMI. We found that altered lysophosphatidylcholine (LPC) to lysophosphatidylethanolamine (LPE) ratio predicted STEMI and NSTEMI events in different ways. In STEMI, lysophospholipids (mainly LPEs) were lower, whereas in NSTEMI, lysophospholipids (mainly LPEs) were higher. We found a similar response for all detected lysophospholipids but significant alterations only for those containing linoleic acid (C18:2, p < 0.05). Patients with STEMI had higher secretoglobin family 3A member 2 and tartrate-resistant acid phosphate type 5 and lower platelet-derived growth factor subunit A, which are proteins associated with atherosclerosis severity and plaque development mediated via altered phospholipid metabolism. In contrast, patients with NSTEMI had higher levels of proteins associated with inflammation and macrophage activation, including interleukin 6, C-reactive protein, chemerin, and cathepsin X and D. The STEMI risk marker profile includes factors closely related to the development of unstable plaque, including a higher LPC:LPE ratio, whereas NSTEMI is characterized by a lower LPC:LPE ratio and increased inflammation.
Published: 2020
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34. Von Willebrand factor, ABO blood group, and risk of first-ever intracerebral hemorrhage: A prospective nested case-control study.

Author: Johansson K, Jansson JH, Johansson L, Ekblom K, and Lind MM
Subjects: Adult, Case-Control Studies, Cerebral Hemorrhage, Female, Humans, Male, Middle Aged, Prospective Studies, ABO Blood-Group System, von Willebrand Factor
Abstract: Background and Purpose: Low levels of von Willebrand factor (VWF) were associated with intracerebral hemorrhage (ICH) in a previous study. Persons with blood group O have lower VWF levels than other ABO blood groups. This study aimed to investigate the association between VWF and the risk of ICH in adults, as well as the association between ABO blood group and risk of ICH., Methods: This population-based, nested case-control study was conducted using data and blood samples from health examinations between 1985 and 2007. All participants were followed, and cases with first-ever ICH were identified and validated. One or two controls were matched to each case., Results: During a median follow-up time from blood sampling to ICH of 5.6 years, 176 cases with ICH were identified. The mean age at health examination was 57 years; 50% of participants were women. There was an association between hypertension and risk of ICH, but there was no association between VWF level and risk of ICH. There was no association between blood group O and risk of ICH., Conclusions: To our knowledge this is the largest prospective study investigating the association between VWF, ABO blood group and ICH. We found no association between VWF or blood group O and risk of future ICH., (Copyright © 2020 Elsevier Ltd. All rights reserved.)
Published: 2020
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35. Meta-analysis of up to 622,409 individuals identifies 40 novel smoking behaviour associated genetic loci.

Author: Erzurumluoglu AM, Liu M, Jackson VE, Barnes DR, Datta G, Melbourne CA, Young R, Batini C, Surendran P, Jiang T, Adnan SD, Afaq S, Agrawal A, Altmaier E, Antoniou AC, Asselbergs FW, Baumbach C, Bierut L, Bertelsen S, Boehnke M, Bots ML, Brazel DM, Chambers JC, Chang-Claude J, Chen C, Corley J, Chou YL, David SP, de Boer RA, de Leeuw CA, Dennis JG, Dominiczak AF, Dunning AM, Easton DF, Eaton C, Elliott P, Evangelou E, Faul JD, Foroud T, Goate A, Gong J, Grabe HJ, Haessler J, Haiman C, Hallmans G, Hammerschlag AR, Harris SE, Hattersley A, Heath A, Hsu C, Iacono WG, Kanoni S, Kapoor M, Kaprio J, Kardia SL, Karpe F, Kontto J, Kooner JS, Kooperberg C, Kuulasmaa K, Laakso M, Lai D, Langenberg C, Le N, Lettre G, Loukola A, Luan J, Madden PAF, Mangino M, Marioni RE, Marouli E, Marten J, Martin NG, McGue M, Michailidou K, Mihailov E, Moayyeri A, Moitry M, Müller-Nurasyid M, Naheed A, Nauck M, Neville MJ, Nielsen SF, North K, Perola M, Pharoah PDP, Pistis G, Polderman TJ, Posthuma D, Poulter N, Qaiser B, Rasheed A, Reiner A, Renström F, Rice J, Rohde R, Rolandsson O, Samani NJ, Samuel M, Schlessinger D, Scholte SH, Scott RA, Sever P, Shao Y, Shrine N, Smith JA, Starr JM, Stirrups K, Stram D, Stringham HM, Tachmazidou I, Tardif JC, Thompson DJ, Tindle HA, Tragante V, Trompet S, Turcot V, Tyrrell J, Vaartjes I, van der Leij AR, van der Meer P, Varga TV, Verweij N, Völzke H, Wareham NJ, Warren HR, Weir DR, Weiss S, Wetherill L, Yaghootkar H, Yavas E, Jiang Y, Chen F, Zhan X, Zhang W, Zhao W, Zhao W, Zhou K, Amouyel P, Blankenberg S, Caulfield MJ, Chowdhury R, Cucca F, Deary IJ, Deloukas P, Di Angelantonio E, Ferrario M, Ferrières J, Franks PW, Frayling TM, Frossard P, Hall IP, Hayward C, Jansson JH, Jukema JW, Kee F, Männistö S, Metspalu A, Munroe PB, Nordestgaard BG, Palmer CNA, Salomaa V, Sattar N, Spector T, Strachan DP, van der Harst P, Zeggini E, Saleheen D, Butterworth AS, Wain LV, Abecasis GR, Danesh J, Tobin MD, Vrieze S, Liu DJ, and Howson JMM
Subjects: Biological Specimen Banks, Databases, Factual, Europe ethnology, Exome, Female, Humans, Male, Polymorphism, Single Nucleotide genetics, United Kingdom, Genetic Loci, Smoking genetics
Abstract: Smoking is a major heritable and modifiable risk factor for many diseases, including cancer, common respiratory disorders and cardiovascular diseases. Fourteen genetic loci have previously been associated with smoking behaviour-related traits. We tested up to 235,116 single nucleotide variants (SNVs) on the exome-array for association with smoking initiation, cigarettes per day, pack-years, and smoking cessation in a fixed effects meta-analysis of up to 61 studies (up to 346,813 participants). In a subset of 112,811 participants, a further one million SNVs were also genotyped and tested for association with the four smoking behaviour traits. SNV-trait associations with P < 5 × 10 -8 in either analysis were taken forward for replication in up to 275,596 independent participants from UK Biobank. Lastly, a meta-analysis of the discovery and replication studies was performed. Sixteen SNVs were associated with at least one of the smoking behaviour traits (P < 5 × 10 -8 ) in the discovery samples. Ten novel SNVs, including rs12616219 near TMEM182, were followed-up and five of them (rs462779 in REV3L, rs12780116 in CNNM2, rs1190736 in GPR101, rs11539157 in PJA1, and rs12616219 near TMEM182) replicated at a Bonferroni significance threshold (P < 4.5 × 10 -3 ) with consistent direction of effect. A further 35 SNVs were associated with smoking behaviour traits in the discovery plus replication meta-analysis (up to 622,409 participants) including a rare SNV, rs150493199, in CCDC141 and two low-frequency SNVs in CEP350 and HDGFRP2. Functional follow-up implied that decreased expression of REV3L may lower the probability of smoking initiation. The novel loci will facilitate understanding the genetic aetiology of smoking behaviour and may lead to the identification of potential drug targets for smoking prevention and/or cessation.
Published: 2020
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36. GDF-15 is associated with sudden cardiac death due to incident myocardial infarction.

Author: Andersson J, Fall T, Delicano R, Wennberg P, and Jansson JH
Subjects: Biomarkers, Case-Control Studies, Death, Sudden, Cardiac epidemiology, Death, Sudden, Cardiac etiology, Humans, Prospective Studies, Proteomics, Risk Factors, Sweden epidemiology, Growth Differentiation Factor 15, Myocardial Infarction complications
Abstract: Aims: Preventing sudden cardiac death (SCD) due to acute myocardial infarction (MI) in previously healthy patients is challenging. Proteomic analysis may lead to an understanding of biological mechanisms and provide predictive biomarkers., Methods: In this prospective, nested case-control study from northern Sweden, 87 candidate cardiovascular protein biomarkers were studied in 244 individuals who later died within 24 h from an incident MI and 244 referents without MI and individually matched for age, sex and date of health examination and alive at the date of event in the index person. Association analysis was conducted using conditional logistic regression. Bonferroni correction was applied to avoid false positive findings., Results: Ten proteins were associated with future SCD due to acute MI in the non-adjusted analysis. The strongest association were found for growth differentiation factor 15 (GDF-15) with an odds ratio (OR) of 1.79 (95% confidence interval [CI] 1.41, 2.25) per standard deviation increase in protein, and urokinase-type plasminogen activator receptor with an OR of 1.66 (95% CI 1.34, 2.06). In models adjusted for lipid levels, body mass index, education, smoking, hypertension and C-reactive protein, only association with GDF-15 remained (OR 1.47 (95% 1.11, 1.95))., Conclusion: Elevated levels of GDF-15 are associated with increased risk of SCD within 24 h of incident MI. Further research may enable the use of GDF-15 together with other clinical and biological markers to guide primary preventive interventions for individuals at high risk for SCD., (Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.)
Published: 2020
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37. Leptin levels are not affected by enalapril treatment after an uncomplicated myocardial infarction, but associate strongly with changes in fibrinolytic variables in men.

Author: Eriksson MA, Söderberg S, Nilsson TK, Eriksson M, Boman K, and Jansson JH
Subjects: Aged, Angiotensin-Converting Enzyme Inhibitors therapeutic use, Antihypertensive Agents therapeutic use, Double-Blind Method, Female, Fibrinolysis drug effects, Gene Expression Regulation, Humans, Leptin genetics, Male, Middle Aged, Myocardial Infarction complications, Myocardial Infarction drug therapy, Myocardial Infarction genetics, Obesity complications, Obesity drug therapy, Obesity genetics, Plasminogen Activator Inhibitor 1 genetics, Protein Binding, Sex Factors, Signal Transduction, Tissue Plasminogen Activator genetics, Enalapril therapeutic use, Leptin blood, Myocardial Infarction blood, Obesity blood, Plasminogen Activator Inhibitor 1 blood, Tissue Plasminogen Activator blood
Abstract: Leptin, an adipocyte-derived hormone, is involved in the regulation of body weight and is associated with obesity-related complications, notably cardiovascular disease (CVD). A putative link between obesity and CVD could be induction of plasminogen activator inhibitor-1 (PAI-1) synthesis by leptin. In this study, we hypothesized that the beneficial effect of the angiotensin-converting enzyme inhibitor (ACE i ) enalapril on PAI-1 levels is mediated by effects on leptin levels. The association between leptin and components of the fibrinolytic system was evaluated in a non-prespecified post hoc analysis of a placebo-controlled randomized, double-blind trial where the effect of the ACE i enalapril on fibrinolysis was tested. A total of 46 men and 37 women were randomized to treatment with enalapril or placebo after (median 12 months) an uncomplicated myocardial infarction. At baseline, the participants were stable and had no signs of congestive heart failure. Leptin and fibrinolytic variables (mass concentrations of PAI-1, tissue plasminogen activator (tPA) and tPA-PAI complex) were measured at baseline, and after 10 days, 6 months and 12 months. Enalapril treatment did not change leptin levels, which increased significantly during 1 year of follow-up ( p = .007). Changes in leptin levels were strongly associated with changes of tPA mass ( p = .001), tPA-PAI complex ( p = .003) and of PAI-1 ( p = .006) in men, but not in women. Leptin levels are not influenced by treatment with an ACE i . In contrast, leptin associates strongly with changes in fibrinolytic variables notably with a sex difference, which could be of importance for obesity-related CVD.
Published: 2020
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38. Phosphatidylethanol Levels, As a Marker of Alcohol Consumption, Are Associated With Risk of Intracerebral Hemorrhage.

Author: Johansson K, Johansson L, Pennlert J, Söderberg S, Jansson JH, and Lind MM
Subjects: Adult, Aged, Alcohol Drinking blood, Case-Control Studies, Female, Humans, Male, Middle Aged, Prospective Studies, Sweden, Alcohol Drinking adverse effects, Biomarkers blood, Cerebral Hemorrhage blood, Cerebral Hemorrhage etiology, Glycerophospholipids blood
Abstract: Background and Purpose: Previous observational studies have shown a moderately increased risk of intracerebral hemorrhage (ICH) with high self-reported alcohol consumption. However, self-reported data tend to underestimate alcohol consumption. Phosphatidylethanol is a specific biomarker reflecting alcohol intake during the last month and correlates with the amount of alcohol consumed. The present study aimed to investigate the association between phosphatidylethanol levels and the risk of future ICH., Methods: This population-based nested case-referent study was conducted within the Northern Sweden Health and Disease Cohort. At baseline, all participants underwent a health examination, including a questionnaire with questions about alcohol consumption. A blood sample was collected and stored at -80°C, and phosphatidylethanol 16:0/18:1 levels were measured in packed erythrocytes. Cases (n=97) were diagnosed with a first-ever ICH between 1985 and 2007. Two referents (n=180) were matched to each case., Results: The mean age at baseline was 55 years, 39% of participants were women, and the mean time from blood sampling to ICH was 7.3 years. Only phosphatidylethanol and hypertension remained independently associated with ICH in a multivariable model. Participants with phosphatidylethanol >0.30 μmol/L had an increased risk of ICH compared with those with phosphatidylethanol <0.01 μmol/L (odds ratio, 4.64 [95% CI, 1.49-14.40])., Conclusions: High blood concentrations of phosphatidylethanol were associated with an increased risk of future ICH. This association was independent of hypertension and other risk factors for ICH. Our findings suggest that phosphatidylethanol, as a marker of alcohol consumption, may be used as a risk marker of future ICH.
Published: 2020
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39. High frequency of intermediary alleles in the HTT gene in Northern Sweden - The Swedish Huntingtin Alleles and Phenotype (SHAPE) study.

Author: Sundblom J, Niemelä V, Ghazarian M, Strand AS, Bergdahl IA, Jansson JH, Söderberg S, and Stattin EL
Subjects: Adult, Aged, Female, Humans, Huntington Disease genetics, Male, Middle Aged, Sweden, Trinucleotide Repeats, Gene Frequency, Huntingtin Protein genetics, Phenotype
Abstract: Trinucleotide (CAG) repeat expansions longer than 39 in the huntingtin (HTT) gene cause Huntington's disease (HD). The frequency of intermediate alleles (IA) with a length of 27-35 in the general population is not fully known, but studied in specific materials connected to the incidence of HD. The Swedish Huntingtin Alleles and Phenotype (SHAPE) study aims to assess the frequency of trinucleotide repeat expansions in the HTT gene in north Sweden. 8260 individuals unselected for HD from the counties of Norr- and Västerbotten in the north of Sweden were included. DNA samples were obtained and analysis of the HTT gene was performed, yielding data on HTT gene expansion length in 7379 individuals. A high frequency of intermediate alleles, 6.8%, was seen. Also, individuals with repeat numbers lower than ever previously reported (<5) were found. These results suggest a high frequency of HD in the norther parts of Sweden. Subsequent analyses may elucidate the influence of IA:s on traits other than HD.
Published: 2020
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40. Weight gain and blood pressure.

Author: Sundström J, Lind L, Lampa E, Angerås O, Bachus E, Bergström G, Carlberg B, Engström G, Engvall JE, Eriksson M, Gigante B, Hagström E, Hjelmgren O, Jansson JH, Jernberg T, Mannila M, Nyström FH, Oldgren J, Persson M, Sandström A, Swahn E, Söderberg S, Torén K, Östgren CJ, and Rosengren A
Subjects: Aging, Cohort Studies, Female, Humans, Male, Middle Aged, Self Report, Blood Pressure physiology, Weight Gain physiology
Abstract: Objective: Although the causality of the obesity--hypertension association is established, the potential for prevention is not. We hypothesized that weight gain between early adulthood and mid-life is associated with higher mid-life blood pressure., Methods: We investigated the hypothesis using a large contemporaneous population-based mid-life cohort of men and women aged 50-64 years. Recalled body weight at age 20 years was self-reported, and mid-life body weight and office blood pressures were measured in accordance with a detailed protocol., Results: On average, men had gained 14.9 (95% CI 14.6-15.2) kg of weight, and women 14.6 (95% CI 14.4-14.9) kg, between age 20 years and the mid-life examination, corresponding to 0.40 (95% CI 0.39-0.41) kg/year for men and women. Both weight at age 20 years and weight at the mid-life examination were associated with mid-life blood pressures. On average, a 10 kg weight increase between age 20 years and mid-life was associated with 2.2 (95% CI 0.9-3.5) mmHg higher systolic and 1.7 (95% CI 0.9-2.5) mmHg higher diastolic mid-life blood pressure in men, and 3.2 (2.5-4.0) mmHg higher systolic and 2.4 (1.9-2.9) mmHg higher diastolic mid-life blood pressure in women. Mid-life weight was more closely associated than weight at age 20 years with mid-life blood pressure. For a given mid-life weight, blood pressure was higher in persons with higher weight gain from age 20 years., Conclusion: In sum, weight gain between early adulthood and mid-life was associated with higher mid-life blood pressure. The magnitude of the association indicates a potentially great public health impact of strategies to prevent weight gain throughout adulthood.
Published: 2020
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41. Dairy Products and Cancer Risk in a Northern Sweden Population.

Author: Nilsson LM, Winkvist A, Esberg A, Jansson JH, Wennberg P, van Guelpen B, and Johansson I
Subjects: Adult, Animals, Butter adverse effects, Butter statistics & numerical data, Cheese adverse effects, Cheese statistics & numerical data, Cultured Milk Products adverse effects, Cultured Milk Products statistics & numerical data, Dairy Products adverse effects, Diet adverse effects, Diet statistics & numerical data, Female, Humans, Male, Middle Aged, Milk adverse effects, Milk statistics & numerical data, Neoplasms etiology, Proportional Hazards Models, Prospective Studies, Risk Factors, Surveys and Questionnaires, Sweden epidemiology, Dairy Products statistics & numerical data, Neoplasms epidemiology
Abstract: The role of dairy products in cancer is unclear. We assessed consumption of fermented milk, non-fermented milk, cheese, and butter, estimated from semi-quantitative food frequency questionnaires, in relation to prospective risk of breast, prostate, colorectal, smoking-, and obesity-related cancers in 101,235 subjects, including 12,552 cancer cases, in the population-based Northern Sweden Health and Disease Study. Most analyses ( n = 20) rendered null results. In men, we observed an increased prostate cancer risk among high-consumers of cheese (hazard ratio (HR) for highest vs. lowest quintile (Q5-Q1), 1.11; 95% CI, 0.97-1.27; P trend = 0.013). In women, high-consumers of cheese had a decreased risk of overall cancer (HR Q5-Q1, 0.95; 95% CI, 0.88-1.04; P trend = 0.039), smoking-related (HR Q5-Q1, 0.84; 95% CI, 0.72-0.97; P trend ≤ 0.001), and colorectal cancers (HR Q5-Q1, 0.82; 95% CI, 0.63-1.07; P trend = 0.048). Butter yielded a weak decreased obesity-related cancer risk in women (HR Q5-Q1, 0.91; 95% CI, 0.81-1.02; P trend = 0.049). Fermented milk yielded HRs below zero in women, but with no clear linear associations. In conclusion, this study does not support any major adverse or beneficial effects of fermented milk, non-fermented milk, cheese, and butter in the diet from a cancer risk perspective.
Published: 2020
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42. Publisher Correction: Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.

Author: Turcot V, Lu Y, Highland HM, Schurmann C, Justice AE, Fine RS, Bradfield JP, Esko T, Giri A, Graff M, Guo X, Hendricks AE, Karaderi T, Lempradl A, Locke AE, Mahajan A, Marouli E, Sivapalaratnam S, Young KL, Alfred T, Feitosa MF, Masca NGD, Manning AK, Medina-Gomez C, Mudgal P, Ng MCY, Reiner AP, Vedantam S, Willems SM, Winkler TW, Abecasis G, Aben KK, Alam DS, Alharthi SE, Allison M, Amouyel P, Asselbergs FW, Auer PL, Balkau B, Bang LE, Barroso I, Bastarache L, Benn M, Bergmann S, Bielak LF, Blüher M, Boehnke M, Boeing H, Boerwinkle E, Böger CA, Bork-Jensen J, Bots ML, Bottinger EP, Bowden DW, Brandslund I, Breen G, Brilliant MH, Broer L, Brumat M, Burt AA, Butterworth AS, Campbell PT, Cappellani S, Carey DJ, Catamo E, Caulfield MJ, Chambers JC, Chasman DI, Chen YI, Chowdhury R, Christensen C, Chu AY, Cocca M, Collins FS, Cook JP, Corley J, Galbany JC, Cox AJ, Crosslin DS, Cuellar-Partida G, D'Eustacchio A, Danesh J, Davies G, Bakker PIW, Groot MCH, Mutsert R, Deary IJ, Dedoussis G, Demerath EW, Heijer M, Hollander AI, Ruijter HM, Dennis JG, Denny JC, Di Angelantonio E, Drenos F, Du M, Dubé MP, Dunning AM, Easton DF, Edwards TL, Ellinghaus D, Ellinor PT, Elliott P, Evangelou E, Farmaki AE, Farooqi IS, Faul JD, Fauser S, Feng S, Ferrannini E, Ferrieres J, Florez JC, Ford I, Fornage M, Franco OH, Franke A, Franks PW, Friedrich N, Frikke-Schmidt R, Galesloot TE, Gan W, Gandin I, Gasparini P, Gibson J, Giedraitis V, Gjesing AP, Gordon-Larsen P, Gorski M, Grabe HJ, Grant SFA, Grarup N, Griffiths HL, Grove ML, Gudnason V, Gustafsson S, Haessler J, Hakonarson H, Hammerschlag AR, Hansen T, Harris KM, Harris TB, Hattersley AT, Have CT, Hayward C, He L, Heard-Costa NL, Heath AC, Heid IM, Helgeland Ø, Hernesniemi J, Hewitt AW, Holmen OL, Hovingh GK, Howson JMM, Hu Y, Huang PL, Huffman JE, Ikram MA, Ingelsson E, Jackson AU, Jansson JH, Jarvik GP, Jensen GB, Jia Y, Johansson S, Jørgensen ME, Jørgensen T, Jukema JW, Kahali B, Kahn RS, Kähönen M, Kamstrup PR, Kanoni S, Kaprio J, Karaleftheri M, Kardia SLR, Karpe F, Kathiresan S, Kee F, Kiemeney LA, Kim E, Kitajima H, Komulainen P, Kooner JS, Kooperberg C, Korhonen T, Kovacs P, Kuivaniemi H, Kutalik Z, Kuulasmaa K, Kuusisto J, Laakso M, Lakka TA, Lamparter D, Lange EM, Lange LA, Langenberg C, Larson EB, Lee NR, Lehtimäki T, Lewis CE, Li H, Li J, Li-Gao R, Lin H, Lin KH, Lin LA, Lin X, Lind L, Lindström J, Linneberg A, Liu CT, Liu DJ, Liu Y, Lo KS, Lophatananon A, Lotery AJ, Loukola A, Luan J, Lubitz SA, Lyytikäinen LP, Männistö S, Marenne G, Mazul AL, McCarthy MI, McKean-Cowdin R, Medland SE, Meidtner K, Milani L, Mistry V, Mitchell P, Mohlke KL, Moilanen L, Moitry M, Montgomery GW, Mook-Kanamori DO, Moore C, Mori TA, Morris AD, Morris AP, Müller-Nurasyid M, Munroe PB, Nalls MA, Narisu N, Nelson CP, Neville M, Nielsen SF, Nikus K, Njølstad PR, Nordestgaard BG, Nyholt DR, O'Connel JR, O'Donoghue ML, Loohuis LMO, Ophoff RA, Owen KR, Packard CJ, Padmanabhan S, Palmer CNA, Palmer ND, Pasterkamp G, Patel AP, Pattie A, Pedersen O, Peissig PL, Peloso GM, Pennell CE, Perola M, Perry JA, Perry JRB, Pers TH, Person TN, Peters A, Petersen ERB, Peyser PA, Pirie A, Polasek O, Polderman TJ, Puolijoki H, Raitakari OT, Rasheed A, Rauramaa R, Reilly DF, Renström F, Rheinberger M, Ridker PM, Rioux JD, Rivas MA, Roberts DJ, Robertson NR, Robino A, Rolandsson O, Rudan I, Ruth KS, Saleheen D, Salomaa V, Samani NJ, Sapkota Y, Sattar N, Schoen RE, Schreiner PJ, Schulze MB, Scott RA, Segura-Lepe MP, Shah SH, Sheu WH, Sim X, Slater AJ, Small KS, Smith AV, Southam L, Spector TD, Speliotes EK, Starr JM, Stefansson K, Steinthorsdottir V, Stirrups KE, Strauch K, Stringham HM, Stumvoll M, Sun L, Surendran P, Swift AJ, Tada H, Tansey KE, Tardif JC, Taylor KD, Teumer A, Thompson DJ, Thorleifsson G, Thorsteinsdottir U, Thuesen BH, Tönjes A, Tromp G, Trompet S, Tsafantakis E, Tuomilehto J, Tybjaerg-Hansen A, Tyrer JP, Uher R, Uitterlinden AG, Uusitupa M, Laan SW, Duijn CM, Leeuwen N, van Setten J, Vanhala M, Varbo A, Varga TV, Varma R, Edwards DRV, Vermeulen SH, Veronesi G, Vestergaard H, Vitart V, Vogt TF, Völker U, Vuckovic D, Wagenknecht LE, Walker M, Wallentin L, Wang F, Wang CA, Wang S, Wang Y, Ware EB, Wareham NJ, Warren HR, Waterworth DM, Wessel J, White HD, Willer CJ, Wilson JG, Witte DR, Wood AR, Wu Y, Yaghootkar H, Yao J, Yao P, Yerges-Armstrong LM, Young R, Zeggini E, Zhan X, Zhang W, Zhao JH, Zhao W, Zhao W, Zhou W, Zondervan KT, Rotter JI, Pospisilik JA, Rivadeneira F, Borecki IB, Deloukas P, Frayling TM, Lettre G, North KE, Lindgren CM, Hirschhorn JN, and Loos RJF
Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Published: 2019
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43. Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality.

Author: Marklund M, Wu JHY, Imamura F, Del Gobbo LC, Fretts A, de Goede J, Shi P, Tintle N, Wennberg M, Aslibekyan S, Chen TA, de Oliveira Otto MC, Hirakawa Y, Eriksen HH, Kröger J, Laguzzi F, Lankinen M, Murphy RA, Prem K, Samieri C, Virtanen J, Wood AC, Wong K, Yang WS, Zhou X, Baylin A, Boer JMA, Brouwer IA, Campos H, Chaves PHM, Chien KL, de Faire U, Djoussé L, Eiriksdottir G, El-Abbadi N, Forouhi NG, Michael Gaziano J, Geleijnse JM, Gigante B, Giles G, Guallar E, Gudnason V, Harris T, Harris WS, Helmer C, Hellenius ML, Hodge A, Hu FB, Jacques PF, Jansson JH, Kalsbeek A, Khaw KT, Koh WP, Laakso M, Leander K, Lin HJ, Lind L, Luben R, Luo J, McKnight B, Mursu J, Ninomiya T, Overvad K, Psaty BM, Rimm E, Schulze MB, Siscovick D, Skjelbo Nielsen M, Smith AV, Steffen BT, Steffen L, Sun Q, Sundström J, Tsai MY, Tunstall-Pedoe H, Uusitupa MIJ, van Dam RM, Veenstra J, Monique Verschuren WM, Wareham N, Willett W, Woodward M, Yuan JM, Micha R, Lemaitre RN, Mozaffarian D, and Risérus U
Subjects: Aged, Female, Humans, Male, Middle Aged, Biomarkers blood, Nutritive Value, Observational Studies as Topic, Protective Factors, Recommended Dietary Allowances, Risk Assessment, Risk Factors, Arachidonic Acid blood, Cardiovascular Diseases blood, Cardiovascular Diseases diagnosis, Cardiovascular Diseases mortality, Cardiovascular Diseases prevention & control, Diet, Healthy, Dietary Fats administration & dosage, Dietary Fats blood, Linoleic Acid administration & dosage, Linoleic Acid blood, Primary Prevention methods, Risk Reduction Behavior
Abstract: Background: Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies., Methods: We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance-weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available)., Results: In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15 198 incident cardiovascular events occurred among 68 659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88-0.99), 0.78 (0.70-0.85), and 0.88 (0.79-0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88-1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extreme quintiles, higher levels were associated with lower risk of total CVD (0.92; 0.86-0.99). No consistent heterogeneity by population subgroups was identified in the observed relationships., Conclusions: In pooled global analyses, higher in vivo circulating and tissue levels of LA and possibly AA were associated with lower risk of major cardiovascular events. These results support a favorable role for LA in CVD prevention.
Published: 2019
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44. Dairy Product Intake and Cardiometabolic Diseases in Northern Sweden: A 33-Year Prospective Cohort Study.

Author: Johansson I, Esberg A, Nilsson LM, Jansson JH, Wennberg P, and Winkvist A
Subjects: Adult, Aged, Cohort Studies, Diabetes Mellitus, Type 2 epidemiology, Diet, Female, Humans, Male, Middle Aged, Myocardial Infarction epidemiology, Prospective Studies, Stroke epidemiology, Sweden epidemiology, Dairy Products, Diabetes Mellitus, Type 2 etiology, Myocardial Infarction etiology, Stroke etiology
Abstract: Dairy products are important constituents of most diets, and their association with adverse health outcomes remains a focus. We characterized dairy food intake and examined associations with the incidence of type 2 diabetes (T2D), myocardial infarction (MI) or stroke among 108,065 Swedish men and women. Hazard ratios (HRs) and 95% CIs were estimated using the multivariable Cox proportional hazards models in a population characterized by high milk tolerance. During a mean follow-up of 14.2 years, 11,641 first-time events occurred. Non-fermented milk intake decreased, whereas butter intake increased over the period. For high intake of non-fermented milk, the HR (95% CI) for developing T2D and MI was 1.17 (1.03, 1.34) and 1.23 (1.10, 1.37), respectively, in men. A greater intake of butter, fermented milk, and cheese tended to be associated with a reduced risk of T2D and/or MI. Non-consumers and those who chose low-fat variants of the targeted dairy products had increased risk for T2D, MI, or stroke compared to those in the non-case group. Generally, effect-sizes were small. This prospective study found that non-fermented milk was associated with an increased risk for developing T2D and MI and that subjects abstaining from dairy products or choosing low-fat variants were at greater risk. However, the overall cardiometabolic risk of non-fermented milk intake was judged as low, since the effect sizes were small., Competing Interests: The authors declare no conflict of interest, and the funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results
Published: 2019
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45. The association between circulating endostatin levels and incident myocardial infarction.

Author: Ruge T, Carlsson AC, Jansson JH, Söderberg S, Larsson A, and Ärnlöv J
Subjects: Adult, Aged, Biomarkers blood, C-Reactive Protein analysis, Case-Control Studies, Female, Humans, Incidence, Male, Middle Aged, Myocardial Infarction diagnosis, Prognosis, Prospective Studies, Registries, Risk Assessment, Risk Factors, Sex Factors, Sweden epidemiology, Time Factors, Up-Regulation, Endostatins blood, Myocardial Infarction blood, Myocardial Infarction epidemiology
Abstract: Objective: Increased levels of circulating endostatin have been observed in patients with prevalent ischemic heart disease. However, the association between circulating endostatin, and incident myocardial infarction (MI) is less studied. Our main aim was to study the association between circulating endostatin and incident MI in the community adjusted for established cardiovascular risk factors in men and women., Design: Circulating endostatin was measured in a nested case control study based on three large community-based Swedish cohorts, including 533 MI cases, and 1003 age-, sex- and cohort-matched controls. Odds ratios (OR) with 95% confidence intervals (CI) were calculated with adjustments for established cardiovascular risk factors., Results: Higher endostatin was associated with a higher incidence of MI independently of established cardiovascular risk factors (OR 1.19, 95% CI 1.03-1.37, p = .02), but this association was abolished after additional adjustment for C-reactive protein. Sex-stratified analyses suggest that the association was substantially stronger in women as compared to men., Conclusions: In our community based sample, higher endostatin predicted incident myocardial infarction predominantly in women but not independently of CRP. Thus, our findings do not support a broad utility of endostatin measurements for the prediction of incident myocardial infarction in clinical practice.
Published: 2018
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46. Dairy intake revisited - associations between dairy intake and lifestyle related cardio-metabolic risk factors in a high milk consuming population.

Author: Johansson I, Nilsson LM, Esberg A, Jansson JH, and Winkvist A
Subjects: Adult, Animals, Cross-Sectional Studies, Dairy Products, Diet methods, Diet statistics & numerical data, Female, Humans, Longitudinal Studies, Male, Middle Aged, Risk Factors, Sweden, Blood Glucose, Blood Pressure physiology, Body Mass Index, Cholesterol blood, Life Style, Milk statistics & numerical data, Triglycerides blood
Abstract: Background: The association between milk and dairy intake and the incidence of cardiometabolic diseases, cancer and mortality has been evaluated in many studies, but these studies have had conflicting results with no clear conclusion on causal or confounding associations. The present study aims to further address this association by cross-sectional and longitudinal evaluation of the associations between exposure to various types of dairy products and metabolic risk markers among inhabitants in northern Sweden while taking other lifestyle factors into account., Methods: Respondents in the Västerbotten Intervention Programme with complete and plausible diet data between 1991 and 2016 were included, yielding 124,934 observations from 90,512 unique subjects. For longitudinal analysis, 27,682 participants with a visit 8-12 years after the first visit were identified. All participants completed a validated Food Frequency Questionnaire. Metabolic risk markers, including body mass index (BMI), blood pressure, serum (S) cholesterol and triglycerides, and blood glucose, were measured. Participants were categorized into quintiles by intake of dairy products, and risk (odds ratios, OR) of undesirable levels of metabolic risk markers was assessed in multivariable logistic regression analyses. In longitudinal analyses, intake quintiles were related to desirable levels of metabolic risk markers at both visits or deterioration at follow-up using Cox regression analyses., Results: The OR of being classified with an undesirable BMI decreased with increasing quintiles of total dairy, cheese and butter intake but increased with increasing non-fermented milk intake. The OR of being classified with an undesirable S-cholesterol level increased with increasing intake of total dairy, butter and high fat (3%) non-fermented milk, whereas an undesirable S-triglyceride level was inversely associated with cheese and butter intake in women. In longitudinal analyses, increasing butter intake was associated with deterioration of S-cholesterol and blood glucose levels, whereas increasing cheese intake was associated with a lower risk of deterioration of S-triglycerides., Conclusions: Confounding factors likely contribute to the demonstrated association between dairy intake and mortality, and other medical conditions and analyses should be stratified by dairy type.
Published: 2018
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47. A comprehensive evaluation of the genetic architecture of sudden cardiac arrest.

Author: Ashar FN, Mitchell RN, Albert CM, Newton-Cheh C, Brody JA, Müller-Nurasyid M, Moes A, Meitinger T, Mak A, Huikuri H, Junttila MJ, Goyette P, Pulit SL, Pazoki R, Tanck MW, Blom MT, Zhao X, Havulinna AS, Jabbari R, Glinge C, Tragante V, Escher SA, Chakravarti A, Ehret G, Coresh J, Li M, Prineas RJ, Franco OH, Kwok PY, Lumley T, Dumas F, McKnight B, Rotter JI, Lemaitre RN, Heckbert SR, O'Donnell CJ, Hwang SJ, Tardif JC, VanDenburgh M, Uitterlinden AG, Hofman A, Stricker BHC, de Bakker PIW, Franks PW, Jansson JH, Asselbergs FW, Halushka MK, Maleszewski JJ, Tfelt-Hansen J, Engstrøm T, Salomaa V, Virmani R, Kolodgie F, Wilde AAM, Tan HL, Bezzina CR, Eijgelsheim M, Rioux JD, Jouven X, Kääb S, Psaty BM, Siscovick DS, Arking DE, and Sotoodehnia N
Subjects: Arrhythmias, Cardiac physiopathology, Body Mass Index, Coronary Artery Disease genetics, Female, Genome-Wide Association Study, Heart Conduction System physiopathology, Humans, Male, Mendelian Randomization Analysis, Polymorphism, Single Nucleotide, Risk Assessment methods, Risk Factors, Sex Factors, Arrhythmias, Cardiac genetics, Death, Sudden, Cardiac etiology
Abstract: Aims: Sudden cardiac arrest (SCA) accounts for 10% of adult mortality in Western populations. We aim to identify potential loci associated with SCA and to identify risk factors causally associated with SCA., Methods and Results: We carried out a large genome-wide association study (GWAS) for SCA (n = 3939 cases, 25 989 non-cases) to examine common variation genome-wide and in candidate arrhythmia genes. We also exploited Mendelian randomization (MR) methods using cross-trait multi-variant genetic risk score associations (GRSA) to assess causal relationships of 18 risk factors with SCA. No variants were associated with SCA at genome-wide significance, nor were common variants in candidate arrhythmia genes associated with SCA at nominal significance. Using cross-trait GRSA, we established genetic correlation between SCA and (i) coronary artery disease (CAD) and traditional CAD risk factors (blood pressure, lipids, and diabetes), (ii) height and BMI, and (iii) electrical instability traits (QT and atrial fibrillation), suggesting aetiologic roles for these traits in SCA risk., Conclusions: Our findings show that a comprehensive approach to the genetic architecture of SCA can shed light on the determinants of a complex life-threatening condition with multiple influencing factors in the general population. The results of this genetic analysis, both positive and negative findings, have implications for evaluating the genetic architecture of patients with a family history of SCA, and for efforts to prevent SCA in high-risk populations and the general community.
Published: 2018
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48. D-Dimer Is Associated With First-Ever Intracerebral Hemorrhage.

Author: Johansson K, Jansson JH, Johansson L, Wiklund PG, Nilsson TK, and Lind M
Subjects: Case-Control Studies, Cerebral Hemorrhage blood, Female, Humans, Male, Middle Aged, Multivariate Analysis, Odds Ratio, Sweden epidemiology, Time Factors, Cerebral Hemorrhage epidemiology, Fibrin Fibrinogen Degradation Products metabolism
Abstract: Background and Purpose- Hypertension is the most important risk factor for intracerebral hemorrhage (ICH), but further characterization is needed for groups at high risk of ICH. One way to predict the risk of developing a disease is with plasma biomarkers. This study aimed to investigate the association between the biomarker, D-dimer, and ICH risk. Methods- This population-based, nested case-control study was conducted using data from 2 population-based surveys; the Västerbotten Intervention Programme and MONICA Northern Sweden (Monitoring Trends and Determinants in Cardiovascular Disease). All participants underwent a health examination and blood sampling at baseline before the event. Cases (n=141) were diagnosed with a first-ever ICH between 1985 and March 2007. One or 2 controls (n=255) were matched to each case. Results- The median age was 60 years; 39% of participants were women; and the median time from blood sampling to ICH was 5.2 years. When D-dimer was evaluated as a continuous variable, it was significantly associated with ICH. After multivariable adjustment (for hypertension, body mass index, cholesterol levels, diabetes mellitus, and smoking), the odds ratio was 1.36 per SD of D-dimer (95% CI, 1.05-1.77). When participants were stratified in 3 groups according to time from blood sampling at health examination to ICH, we found that the association between D-dimer levels and ICH was most pronounced in individuals with the shortest time from blood sampling to ICH event (<3.5 years; odds ratio, 1.78; 95% CI, 1.05-3.05). Conclusions- High plasma concentrations of D-dimer were associated with increased risk of a future ICH, after adjusting for cardiovascular risk factors. This association was predominantly driven by the cases with the shortest time from blood sampling to ICH event.
Published: 2018
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49. Levels of soluble tumor necrosis factor receptor 1 and 2, gender, and risk of myocardial infarction in Northern Sweden.

Author: Carlsson AC, Jansson JH, Söderberg S, Ruge T, Larsson A, and Ärnlöv J
Subjects: Adult, Anthropometry, C-Reactive Protein analysis, Case-Control Studies, Female, Humans, Inflammation, Male, Middle Aged, Odds Ratio, Prospective Studies, Risk Factors, Sex Factors, Sweden epidemiology, Coronary Disease blood, Myocardial Infarction blood, Receptors, Tumor Necrosis Factor, Type I blood, Receptors, Tumor Necrosis Factor, Type II blood
Abstract: Background and Aims: Soluble receptors for tumor necrosis factor alpha (sTNFR1 and sTNFR2) have been associated with cardiovascular diseases, and some evidence points towards a difference in associated risk between men and women. We aimed to study the association between sTNFR1 and sTNFR2 and incident myocardial infarctions (MI) and to explore the influence of established cardiovascular risk factors in men and women., Methods: We conducted a nested case control study in three large Swedish cohorts, including 533 myocardial infarction cases, and 1003 age-, sex- and cohort-matched controls. Odds ratios (OR) with 95% confidence intervals (CI) were calculated., Results: An association between circulating sTNFR1 and sTNFR2 and an increased risk for MI was found when comparing cases and controls. The odds ratios were significant after adjustment for established cardiovascular risk factors and C-reactive protein in women (OR 1.44, 95% CI 1.08-1.93 for TNFR1, and 1.61, 95% CI 1.11-2.34 for TNFR2), but was abolished in men. Women with a combination of elevated CRP and values in the upper quartile of TNFR1 or TNFR2 had a 5-fold higher risk of myocardial infarction versus those with normal CRP and values in the lower three quartiles of TNFR1 or TNFR2., Conclusions: As the risk estimates for TNFR1 and TNFR2 were higher and remained significant after adjustments for established cardiovascular risk factors in women but not in men, a potential role for TNFR1 and TNFR2 in identifying women with a higher MI risk is possible. The future clinical role of TNFR1 and TNFR2 in combination with CRP to identify high risk patients for coronary heart disease has yet to be determined., (Copyright © 2018 Elsevier B.V. All rights reserved.)
Published: 2018
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50. Publisher Correction: Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.

Author: Turcot V, Lu Y, Highland HM, Schurmann C, Justice AE, Fine RS, Bradfield JP, Esko T, Giri A, Graff M, Guo X, Hendricks AE, Karaderi T, Lempradl A, Locke AE, Mahajan A, Marouli E, Sivapalaratnam S, Young KL, Alfred T, Feitosa MF, Masca NGD, Manning AK, Medina-Gomez C, Mudgal P, Ng MCY, Reiner AP, Vedantam S, Willems SM, Winkler TW, Abecasis G, Aben KK, Alam DS, Alharthi SE, Allison M, Amouyel P, Asselbergs FW, Auer PL, Balkau B, Bang LE, Barroso I, Bastarache L, Benn M, Bergmann S, Bielak LF, Blüher M, Boehnke M, Boeing H, Boerwinkle E, Böger CA, Bork-Jensen J, Bots ML, Bottinger EP, Bowden DW, Brandslund I, Breen G, Brilliant MH, Broer L, Brumat M, Burt AA, Butterworth AS, Campbell PT, Cappellani S, Carey DJ, Catamo E, Caulfield MJ, Chambers JC, Chasman DI, Chen YI, Chowdhury R, Christensen C, Chu AY, Cocca M, Collins FS, Cook JP, Corley J, Corominas Galbany J, Cox AJ, Crosslin DS, Cuellar-Partida G, D'Eustacchio A, Danesh J, Davies G, Bakker PIW, Groot MCH, Mutsert R, Deary IJ, Dedoussis G, Demerath EW, Heijer M, Hollander AI, Ruijter HM, Dennis JG, Denny JC, Angelantonio E, Drenos F, Du M, Dubé MP, Dunning AM, Easton DF, Edwards TL, Ellinghaus D, Ellinor PT, Elliott P, Evangelou E, Farmaki AE, Farooqi IS, Faul JD, Fauser S, Feng S, Ferrannini E, Ferrieres J, Florez JC, Ford I, Fornage M, Franco OH, Franke A, Franks PW, Friedrich N, Frikke-Schmidt R, Galesloot TE, Gan W, Gandin I, Gasparini P, Gibson J, Giedraitis V, Gjesing AP, Gordon-Larsen P, Gorski M, Grabe HJ, Grant SFA, Grarup N, Griffiths HL, Grove ML, Gudnason V, Gustafsson S, Haessler J, Hakonarson H, Hammerschlag AR, Hansen T, Harris KM, Harris TB, Hattersley AT, Have CT, Hayward C, He L, Heard-Costa NL, Heath AC, Heid IM, Helgeland Ø, Hernesniemi J, Hewitt AW, Holmen OL, Hovingh GK, Howson JMM, Hu Y, Huang PL, Huffman JE, Ikram MA, Ingelsson E, Jackson AU, Jansson JH, Jarvik GP, Jensen GB, Jia Y, Johansson S, Jørgensen ME, Jørgensen T, Jukema JW, Kahali B, Kahn RS, Kähönen M, Kamstrup PR, Kanoni S, Kaprio J, Karaleftheri M, Kardia SLR, Karpe F, Kathiresan S, Kee F, Kiemeney LA, Kim E, Kitajima H, Komulainen P, Kooner JS, Kooperberg C, Korhonen T, Kovacs P, Kuivaniemi H, Kutalik Z, Kuulasmaa K, Kuusisto J, Laakso M, Lakka TA, Lamparter D, Lange EM, Lange LA, Langenberg C, Larson EB, Lee NR, Lehtimäki T, Lewis CE, Li H, Li J, Li-Gao R, Lin H, Lin KH, Lin LA, Lin X, Lind L, Lindström J, Linneberg A, Liu CT, Liu DJ, Liu Y, Lo KS, Lophatananon A, Lotery AJ, Loukola A, Luan J, Lubitz SA, Lyytikäinen LP, Männistö S, Marenne G, Mazul AL, McCarthy MI, McKean-Cowdin R, Medland SE, Meidtner K, Milani L, Mistry V, Mitchell P, Mohlke KL, Moilanen L, Moitry M, Montgomery GW, Mook-Kanamori DO, Moore C, Mori TA, Morris AD, Morris AP, Müller-Nurasyid M, Munroe PB, Nalls MA, Narisu N, Nelson CP, Neville M, Nielsen SF, Nikus K, Njølstad PR, Nordestgaard BG, Nyholt DR, O'Connel JR, O'Donoghue ML, Olde Loohuis LM, Ophoff RA, Owen KR, Packard CJ, Padmanabhan S, Palmer CNA, Palmer ND, Pasterkamp G, Patel AP, Pattie A, Pedersen O, Peissig PL, Peloso GM, Pennell CE, Perola M, Perry JA, Perry JRB, Pers TH, Person TN, Peters A, Petersen ERB, Peyser PA, Pirie A, Polasek O, Polderman TJ, Puolijoki H, Raitakari OT, Rasheed A, Rauramaa R, Reilly DF, Renström F, Rheinberger M, Ridker PM, Rioux JD, Rivas MA, Roberts DJ, Robertson NR, Robino A, Rolandsson O, Rudan I, Ruth KS, Saleheen D, Salomaa V, Samani NJ, Sapkota Y, Sattar N, Schoen RE, Schreiner PJ, Schulze MB, Scott RA, Segura-Lepe MP, Shah SH, Sheu WH, Sim X, Slater AJ, Small KS, Smith AV, Southam L, Spector TD, Speliotes EK, Starr JM, Stefansson K, Steinthorsdottir V, Stirrups KE, Strauch K, Stringham HM, Stumvoll M, Sun L, Surendran P, Swift AJ, Tada H, Tansey KE, Tardif JC, Taylor KD, Teumer A, Thompson DJ, Thorleifsson G, Thorsteinsdottir U, Thuesen BH, Tönjes A, Tromp G, Trompet S, Tsafantakis E, Tuomilehto J, Tybjaerg-Hansen A, Tyrer JP, Uher R, Uitterlinden AG, Uusitupa M, Laan SW, Duijn CM, Leeuwen N, van Setten J, Vanhala M, Varbo A, Varga TV, Varma R, Velez Edwards DR, Vermeulen SH, Veronesi G, Vestergaard H, Vitart V, Vogt TF, Völker U, Vuckovic D, Wagenknecht LE, Walker M, Wallentin L, Wang F, Wang CA, Wang S, Wang Y, Ware EB, Wareham NJ, Warren HR, Waterworth DM, Wessel J, White HD, Willer CJ, Wilson JG, Witte DR, Wood AR, Wu Y, Yaghootkar H, Yao J, Yao P, Yerges-Armstrong LM, Young R, Zeggini E, Zhan X, Zhang W, Zhao JH, Zhao W, Zhou W, Zondervan KT, Rotter JI, Pospisilik JA, Rivadeneira F, Borecki IB, Deloukas P, Frayling TM, Lettre G, North KE, Lindgren CM, Hirschhorn JN, and Loos RJF
Abstract: In the published version of this paper, the name of author Emanuele Di Angelantonio was misspelled. This error has now been corrected in the HTML and PDF versions of the article.
Published: 2018
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