@article {8526,
	title = {{Equalization of four cardiovascular risk algorithms after systematic recalibration: individual-participant meta-analysis of 86 prospective studies},
	journal = {Eur Heart J},
	volume = {40},
	year = {2019},
	month = {02},
	pages = {621{\textendash}631},
	abstract = {There is debate about the optimum algorithm for cardiovascular disease (CVD) risk estimation. We conducted head-to-head comparisons of four algorithms recommended by primary prevention guidelines, before and after {\textquoteright}recalibration{\textquoteright}, a method that adapts risk algorithms to take account of differences in the risk characteristics of the populations being studied.\ Using individual-participant data on 360 737 participants without CVD at baseline in 86 prospective studies from 22 countries, we compared the Framingham risk score (FRS), Systematic COronary Risk Evaluation (SCORE), pooled cohort equations (PCE), and Reynolds risk score (RRS). We calculated measures of risk discrimination and calibration, and modelled clinical implications of initiating statin therapy in people judged to be at {\textquoteright}high{\textquoteright} 10 year CVD risk. Original risk algorithms were recalibrated using the risk factor profile and CVD incidence of target populations. The four algorithms had similar risk discrimination. Before recalibration, FRS, SCORE, and PCE over-predicted CVD risk on average by 10\%, 52\%, and 41\%, respectively, whereas RRS under-predicted by 10\%. Original versions of algorithms classified 29-39\% of individuals aged {\^a}{\textperthousand}{\textyen}40 years as high risk. By contrast, recalibration reduced this proportion to 22-24\% for every algorithm. We estimated that to prevent one CVD event, it would be necessary to initiate statin therapy in 44-51 such individuals using original algorithms, in contrast to 37-39 individuals with recalibrated algorithms.\ Before recalibration, the clinical performance of four widely used CVD risk algorithms varied substantially. By contrast, simple recalibration nearly equalized their performance and improved modelled targeting of preventive action to clinical need.},
	author = {Pennells, L. and Kaptoge, S. and Wood, A. and Sweeting, M. and Zhao, X. and White, I. and Burgess, S. and Willeit, P. and Bolton, T. and Moons, K. G. M. and van der Schouw, Y. T. and Selmer, R. and Khaw, K. T. and Gudnason, V. and Assmann, G. and Amouyel, P. and Salomaa, V. and Kivimaki, M. and Nordestgaard, B. G. and Blaha, M. J. and Kuller, L. H. and Brenner, H. and Gillum, R. F. and Meisinger, C. and Ford, I. and Knuiman, M. W. and Rosengren, A. and Lawlor, D. A. and V?lzke, H. and Cooper, C. and Mar?n Iba?ez, A. and Casiglia, E. and Kauhanen, J. and Cooper, J. A. and Rodriguez, B. and Sundstr?m, J. and Barrett-Connor, E. and Dankner, R. and Nietert, P. J. and Davidson, K. W. and Wallace, R. B. and Blazer, D. G. and Bj?rkelund, C. and Donfrancesco, C. and Krumholz, H. M. and Nissinen, A. and Davis, B. R. and Coady, S. and Whincup, P. H. and J?rgensen, T. and Ducimetiere, P. and Trevisan, M. and Engstr?m, G. and Crespo, C. J. and Meade, T. W. and Visser, M. and Kromhout, D. and Kiechl, S. and Daimon, M. and Price, J. F. and G?mez de la C?mara, A. and Wouter Jukema, J. and Lamarche, B. and Onat, A. and Simons, L. A. and Kavousi, M. and Ben-Shlomo, Y. and Gallacher, J. and Dekker, J. M. and Arima, H. and Shara, N. and Tipping, R. W. and Roussel, R. and Brunner, E. J. and Koenig, W. and Sakurai, M. and Pavlovic, J. and Gansevoort, R. T. and Nagel, D. and Goldbourt, U. and Barr, E. L. M. and Palmieri, L. and Nj?lstad, I. and Sato, S. and Monique Verschuren, W. M. and Varghese, C. V. and Graham, I. and Onuma, O. and Greenland, P. and Woodward, M. and Ezzati, M. and Psaty, B. M. and Sattar, N. and Jackson, R. and Ridker, P. M. and Cook, N. R. and D{\textquoteright}Agostino, R. B. and Thompson, S. G. and Danesh, J. and Di Angelantonio, E. and Tipping, R. W. and Simpson, L. M. and Pressel, S. L. and Couper, D. J. and Nambi, V. and Matsushita, K. and Folsom, A. R. and Shaw, J. E. and Magliano, D. J. and Zimmet, P. Z. and Knuiman, M. W. and Whincup, P. H. and Wannamethee, S. G. and Willeit, J. and Santer, P. and Egger, G. and Casas, J. P. and Amuzu, A. and Ben-Shlomo, Y. and Gallacher, J. and Tikhonoff, V. and Casiglia, E. and Sutherland, S. E. and Nietert, P. J. and Cushman, M. and Psaty, B. M. and S?gaard, A. J. and H?heim, L. L. and Ariansen, I. and Tybj?rg-Hansen, A. and Jensen, G. B. and Schnohr, P. and Giampaoli, S. and Vanuzzo, D. and Panico, S. and Palmieri, L. and Balkau, B. and Bonnet, F. and Marre, M. and de la C?mara, A. G. and Rubio Herrera, M. A. and Friedlander, Y. and McCallum, J. and McLachlan, S. and Guralnik, J. and Phillips, C. L. and Khaw, K. T. and Wareham, N. and Sch?ttker, B. and Saum, K. U. and Holleczek, B. and Nissinen, A. and Tolonen, H. and Giampaoli, S. and Donfrancesco, C. and Vartiainen, E. and Jousilahti, P. and Harald, K. and D?Agostino, R. B. and Massaro, J. M. and Pencina, M. and Vasan, R. and Kayama, T. and Kato, T. and Oizumi, T. and Jespersen, J. and M?ller, L. and Bladbjerg, E. M. and Chetrit, A. and Rosengren, A. and Wilhelmsen, L. and Bj?rkelund, C. and Lissner, L. and Nagel, D. and Dennison, E. and Kiyohara, Y. and Ninomiya, T. and Doi, Y. and Rodriguez, B. and Nijpels, G. and Stehouwer, C. D. A. and Sato, S. and Kazumasa, Y. and Iso, H. and Goldbourt, U. and Salomaa, V. and Vartiainen, E. and Kurl, S. and Tuomainen, T. P. and Salonen, J. T. and Visser, M. and Deeg, D. J. H. and Meade, T. W. and Nilsson, P. M. and Hedblad, B. and Melander, O. and De Boer, I. H. and DeFilippis, A. P. and Verschuren, W. M. M. and Sattar, N. and Watt, G. and Meisinger, C. and Koenig, W. and Rosengren, A. and Kuller, L. H. and Tverdal, A. and Gillum, R. F. and Cooper, J. A. and Kirkland, S. and Shimbo, D. and Shaffer, J. and Sato, S. and Kazumasa, Y. and Iso, H. and Ducimetiere, P. and Bakker, S. J. L. and van der Harst, P. and Hillege, H. L. and Crespo, C. J. and Amouyel, P. and Dallongeville, J. and Assmann, G. and Schulte, H. and Trompet, S. and Smit, R. A. J. and Stott, D. J. and van der Schouw, Y. T. and Despr?s, J. P. and Cantin, B. and Dagenais, G. R. and Laughlin, G. and Wingard, D. and Trevisan, M. and Aspelund, T. and Eiriksdottir, G. and Gudmundsson, E. F. and Ikram, A. and van Rooij, F. J. A. and Franco, O. H. and Rueda-Ochoa, O. L. and Muka, T. and Glisic, M. and Tunstall-Pedoe, H. and V?lzke, H. and Howard, B. V. and Zhang, Y. and Jolly, S. and Gallacher, J. and Davey-Smith, G. and Can, G. and Y?ksel, H. and Nakagawa, H. and Morikawa, Y. and Miura, K. and Nj?lstad, I. and Ingelsson, M. and Giedraitis, V. and Ridker, P. M. and Gaziano, J. M. and Kivimaki, M. and Shipley, M. and Brunner, E. J. and Arndt, V. and Brenner, H. and Cook, N. and Ridker, P. M. and Ford, I. and Sattar, N. and Iba?ez, A. M. and Geleijnse, J. M.}
}
@article {8281,
	title = {{A multi-ancestry genome-wide study incorporating gene-smoking interactions identifies multiple new loci for pulse pressure and mean arterial pressure},
	journal = {Hum. Mol. Genet.},
	year = {2019},
	month = {Apr},
	abstract = {Elevated blood pressure (BP), a leading cause of global morbidity and mortality, is influenced by both genetic and lifestyle factors. Cigarette smoking is one such lifestyle factor. Across five ancestries, we performed a genome-wide gene-smoking interaction study of mean arterial pressure (MAP) and pulse pressure (PP) in 129 913 individuals in stage 1 and follow-up analysis in 480 178 additional individuals in stage 2. We report here 136 loci significantly associated with MAP and/or PP. Of these, 61 were previously published through main-effect analysis of BP traits, 37 were recently reported by us for systolic BP and/or diastolic BP through gene-smoking interaction analysis and 38 were newly identified (P < 5 {\~A}{\textemdash} 10-8, false discovery rate < 0.05). We also identified nine new signals near known loci. Of the 136 loci, 8 showed significant interaction with smoking status. They include CSMD1 previously reported for insulin resistance and BP in the spontaneously hypertensive rats. Many of the 38 new loci show biologic plausibility for a role in BP regulation. SLC26A7 encodes a chloride/bicarbonate exchanger expressed in the renal outer medullary collecting duct. AVPR1A is widely expressed, including in vascular smooth muscle cells, kidney, myocardium and brain. FHAD1 is a long non-coding RNA overexpressed in heart failure. TMEM51 was associated with contractile function in cardiomyocytes. CASP9 plays a central role in cardiomyocyte apoptosis. Identified only in African ancestry were 30 novel loci. Our findings highlight the value of multi-ancestry investigations, particularly in studies of interaction with lifestyle factors, where genomic and lifestyle differences may contribute to novel findings.},
	author = {Sung, Y. J. and de Las Fuentes, L. and Winkler, T. W. and Chasman, D. I. and Bentley, A. R. and Kraja, A. T. and Ntalla, I. and Warren, H. R. and Guo, X. and Schwander, K. and Manning, A. K. and Brown, M. R. and Aschard, H. and Feitosa, M. F. and Franceschini, N. and Lu, Y. and Cheng, C. Y. and Sim, X. and Vojinovic, D. and Marten, J. and Musani, S. K. and Kilpel?inen, T. O. and Richard, M. A. and Aslibekyan, S. and Bartz, T. M. and Dorajoo, R. and Li, C. and Liu, Y. and Rankinen, T. and Smith, A. V. and Tajuddin, S. M. and Tayo, B. O. and Zhao, W. and Zhou, Y. and Matoba, N. and Sofer, T. and Alver, M. and Amini, M. and Boissel, M. and Chai, J. F. and Chen, X. and Divers, J. and Gandin, I. and Gao, C. and Giulianini, F. and Goel, A. and Harris, S. E. and Hartwig, F. P. and He, M. and Horimoto, A. R. V. R. and Hsu, F. C. and Jackson, A. U. and Kammerer, C. M. and Kasturiratne, A. and Komulainen, P. and K?hnel, B. and Leander, K. and Lee, W. J. and Lin, K. H. and Luan, J. and Lyytik?inen, L. P. and McKenzie, C. A. and Nelson, C. P. and Noordam, R. and Scott, R. A. and Sheu, W. H. H. and Stan??kov?, A. and Takeuchi, F. and van der Most, P. J. and Varga, T. V. and Waken, R. J. and Wang, H. and Wang, Y. and Ware, E. B. and Weiss, S. and Wen, W. and Yanek, L. R. and Zhang, W. and Zhao, J. H. and Afaq, S. and Alfred, T. and Amin, N. and Arking, D. E. and Aung, T. and Barr, R. G. and Bielak, L. F. and Boerwinkle, E. and Bottinger, E. P. and Braund, P. S. and Brody, J. A. and Broeckel, U. and Cade, B. and Campbell, A. and Canouil, M. and Chakravarti, A. and Cocca, M. and Collins, F. S. and Connell, J. M. and de Mutsert, R. and de Silva, H. J. and D?rr, M. and Duan, Q. and Eaton, C. B. and Ehret, G. and Evangelou, E. and Faul, J. D. and Forouhi, N. G. and Franco, O. H. and Friedlander, Y. and Gao, H. and Gigante, B. and Gu, C. C. and Gupta, P. and Hagenaars, S. P. and Harris, T. B. and He, J. and Heikkinen, S. and Heng, C. K. and Hofman, A. and Howard, B. V. and Hunt, S. C. and Irvin, M. R. and Jia, Y. and Katsuya, T. and Kaufman, J. and Kerrison, N. D. and Khor, C. C. and Koh, W. P. and Koistinen, H. A. and Kooperberg, C. B. and Krieger, J. E. and Kubo, M. and Kutalik, Z. and Kuusisto, J. and Lakka, T. A. and Langefeld, C. D. and Langenberg, C. and Launer, L. J. and Lee, J. H. and Lehne, B. and Levy, D. and Lewis, C. E. and Li, Y. and Lim, S. H. and Liu, C. T. and Liu, J. and Liu, J. and Liu, Y. and Loh, M. and Lohman, K. K. and Louie, T. and M?gi, R. and Matsuda, K. and Meitinger, T. and Metspalu, A. and Milani, L. and Momozawa, Y. and Mosley, T. H. and Nalls, M. A. and Nasri, U. and O{\textquoteright}Connell, J. R. and Ogunniyi, A. and Palmas, W. R. and Palmer, N. D. and Pankow, J. S. and Pedersen, N. L. and Peters, A. and Peyser, P. A. and Polasek, O. and Porteous, D. and Raitakari, O. T. and Renstr?m, F. and Rice, T. K. and Ridker, P. M. and Robino, A. and Robinson, J. G. and Rose, L. M. and Rudan, I. and Sabanayagam, C. and Salako, B. L. and Sandow, K. and Schmidt, C. O. and Schreiner, P. J. and Scott, W. R. and Sever, P. and Sims, M. and Sitlani, C. M. and Smith, B. H. and Smith, J. A. and Snieder, H. and Starr, J. M. and Strauch, K. and Tang, H. and Taylor, K. D. and Teo, Y. Y. and Tham, Y. C. and Uitterlinden, A. G. and Waldenberger, M. and Wang, L. and Wang, Y. X. and Wei, W. B. and Wilson, G. and Wojczynski, M. K. and Xiang, Y. B. and Yao, J. and Yuan, J. M. and Zonderman, A. B. and Becker, D. M. and Boehnke, M. and Bowden, D. W. and Chambers, J. C. and Chen, Y. I. and Weir, D. R. and de Faire, U. and Deary, I. J. and Esko, T. and Farrall, M. and Forrester, T. and Freedman, B. I. and Froguel, P. and Gasparini, P. and Gieger, C. and Horta, B. L. and Hung, Y. J. and Jonas, J. B. and Kato, N. and Kooner, J. S. and Laakso, M. and Lehtim?ki, T. and Liang, K. W. and Magnusson, P. K. E. and Oldehinkel, A. J. and Pereira, A. C. and Perls, T. and Rauramaa, R. and Redline, S. and Rettig, R. and Samani, N. J. and Scott, J. and Shu, X. O. and van der Harst, P. and Wagenknecht, L. E. and Wareham, N. J. and Watkins, H. and Wickremasinghe, A. R. and Wu, T. and Kamatani, Y. and Laurie, C. C. and Bouchard, C. and Cooper, R. S. and Evans, M. K. and Gudnason, V. and Hixson, J. and Kardia, S. L. R. and Kritchevsky, S. B. and Psaty, B. M. and van Dam, R. M. and Arnett, D. K. and Mook-Kanamori, D. O. and Fornage, M. and Fox, E. R. and Hayward, C. and van Duijn, C. M. and Tai, E. S. and Wong, T. Y. and Loos, R. J. F. and Reiner, A. P. and Rotimi, C. N. and Bierut, L. J. and Zhu, X. and Cupples, L. A. and Province, M. A. and Rotter, J. I. and Franks, P. W. and Rice, K. and Elliott, P. and Caulfield, M. J. and Gauderman, W. J. and Munroe, P. B. and Rao, D. C. and Morrison, A. C.}
}
@article {9460,
	title = {{Trans Fatty Acid Biomarkers and Incident Type 2 Diabetes: Pooled Analysis of 12 Prospective Cohort Studies in the Fatty Acids and Outcomes Research Consortium (FORCE)},
	journal = {Diabetes Care},
	volume = {45},
	year = {2022},
	month = {Apr},
	pages = {854{\textendash}863},
	abstract = {Trans fatty acids (TFAs) have harmful biologic effects that could increase the risk of type 2 diabetes (T2D), but evidence remains uncertain. We aimed to investigate the prospective associations of TFA biomarkers and T2D by conducting an individual participant-level pooled analysis.\ 18 years without prevalent diabetes. Each cohort conducted de novo harmonized analyses using a prespecified protocol, and findings were pooled using inverse-variance weighted meta-analysis. Heterogeneity was explored by prespecified between-study and within-study characteristics.\ 0.1).\ Circulating individual trans-18:2 TFA biomarkers were not associated with risk of T2D, while trans-16:1n-9, total trans-18:1, and total trans-18:2 were inversely associated. Findings may reflect the influence of mixed TFA sources (industrial vs. natural ruminant), a general decline in TFA exposure due to policy changes during this period, or the relatively limited range of TFA levels.},
	author = {Lai, H. T. M. and Imamura, F. and Korat, A. V. A. and Murphy, R. A. and Tintle, N. and Bassett, J. K. and Chen, J. and ger, J. and Chien, K. L. and Senn, M. and Wood, A. C. and Forouhi, N. G. and Schulze, M. B. and Harris, W. S. and Vasan, R. S. and Hu, F. and Giles, G. G. and Hodge, A. and Djousse, L. and Brouwer, I. A. and Qian, F. and Sun, Q. and Wu, J. H. Y. and Marklund, M. and Lemaitre, R. N. and Siscovick, D. S. and Fretts, A. M. and Shadyab, A. H. and Manson, J. E. and Howard, B. V. and Robinson, J. G. and Wallace, R. B. and Wareham, N. J. and Chen, Y. I. and Rotter, J. I. and Tsai, M. Y. and Micha, R. and Mozaffarian, D.}
}
