ProfessorPaulElliott

Butterworth AS, Braund PS, Farrall M, Hardwick RJ, Saleheen D, Peden JF, Soranzo N, Chambers JC, Sivapalaratnam S, Kleber ME, Keating B, Qasim A, Klopp N, Erdmann J, Assimes TL, Ball SG, Balmforth AJ, Barnes TA, Basart H, Baumert J, Bezzina CR, Boerwinkle E, Boehm BO, Brocheton J, Bugert P, Cambien F, Clarke R, Codd V, Collins R, Couper D, Cupples LA, de Jong JS, Diemert P, Ejebe K, Elbers CC, Elliott P, Fornage M, Franzosi M-G, Frossard P, Garner S, Goel A, Goodall AH, Hengstenberg C, Hunt SE, Kastelein JJP, Klungel OH, Klueter H, Koch K, Koenig IR, Kooner AS, Laaksonen R, Lathrop M, Li M, Liu K, McPherson R, Musameh MD, Musani S, Nelson CP, O'Donnell CJ, Ongen H, Papanicolaou G, Peters A, Peters BJM, Potter S, Psaty BM, Qu L, Rader DJ, Rasheed A, Rice C, Scott J, Seedorf U, Sehmi JS, Sotoodehnia N, Stark K, Stephens J, van der Schoot CE, van der Schouw YT, Thorsteinsdottir U, Tomaszewski M, van der Harst P, Vasan RS, Wilde AAM, Willenborg C, Winkelmann BR, Zaidi M, Zhang W, Ziegler A, de Bakker PIW, Koenig W, Maerz W, Trip MD, Reilly MP, Kathiresan S, Schunkert H, Hamsten A, Hall AS, Kooner JS, Thompson SG, Thompson JR, Deloukas P, Ouwehand WH, Watkins H, Danesh J, Samani NJet al., 2011, Large-scale gene-centric analysis identifies novel variants for coronary Artery disease, PLoS Genetics, Vol: 7, ISSN: 1553-7390

Coronary artery disease (CAD) has a significant genetic contribution that is incompletely characterized. To complement genome-wide association (GWA) studies, we conducted a large and systematic candidate gene study of CAD susceptibility, including analysis of many uncommon and functional variants. We examined 49,094 genetic variants in ∼2,100 genes of cardiovascular relevance, using a customised gene array in 15,596 CAD cases and 34,992 controls (11,202 cases and 30,733 controls of European descent; 4,394 cases and 4,259 controls of South Asian origin). We attempted to replicate putative novel associations in an additional 17,121 CAD cases and 40,473 controls. Potential mechanisms through which the novel variants could affect CAD risk were explored through association tests with vascular risk factors and gene expression. We confirmed associations of several previously known CAD susceptibility loci (eg, 9p21.3:p<10−33; LPA:p<10−19; 1p13.3:p<10−17) as well as three recently discovered loci (COL4A1/COL4A2, ZC3HC1, CYP17A1:p<5×10−7). However, we found essentially null results for most previously suggested CAD candidate genes. In our replication study of 24 promising common variants, we identified novel associations of variants in or near LIPA, IL5, TRIB1, and ABCG5/ABCG8, with per-allele odds ratios for CAD risk with each of the novel variants ranging from 1.06–1.09. Associations with variants at LIPA, TRIB1, and ABCG5/ABCG8 were supported by gene expression data or effects on lipid levels. Apart from the previously reported variants in LPA, none of the other ∼4,500 low frequency and functional variants showed a strong effect. Associations in South Asians did not differ appreciably from those in Europeans, except for 9p21.3 (per-allele odds ratio: 1.14 versus 1.27 respectively; P for heterogeneity = 0.003). This large-scale gene-centric analysis has identified several novel genes for CAD that relate to diverse bioc

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Pitcher A, Ashby D, Elliott P, Petersen SEet al., 2011, Cardiovascular MRI in clinical trials: expanded applications through novel surrogate endpoints, Heart, Vol: 97, Pages: 1286-1292, ISSN: 1468-201X

Recent advances in cardiovascular magnetic resonance (CMR) now allow the accurate and reproducible measurement of many aspects of cardiac and vascular structure and function, with prognostic data emerging for several key imaging biomarkers. These biomarkers are increasingly used in the evaluation of new drugs, devices and lifestyle modifications for the prevention and treatment of cardiovascular disease. This review outlines a conceptual framework for the application of imaging biomarkers to clinical trials, highlights several important CMR techniques which are in use in randomised studies, and reviews certain aspects of trial design, conduct and interpretation in relation to the use of CMR.

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Kestelooty H, Tzoulaki I, Brown IJ, Chan Q, Wijeyesekera A, Ueshima H, Zhao L, Dyer AR, Unwin RJ, Stamler J, Elliott Pet al., 2011, Relation of Urinary Calcium and Magnesium Excretion to Blood Pressure The International Study of Macro- and Micro-Nutrients and Blood Pressure and the International Cooperative Study on Salt, Other Factors, and Blood Pressure, AMERICAN JOURNAL OF EPIDEMIOLOGY, Vol: 174, Pages: 44-51, ISSN: 0002-9262

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• Citations: 39

Desrivieres S, Lourdusamy A, Mueller C, Ducci F, Wong CP, Kaakinen M, Pouta A, Hartikainen A-L, Isohanni M, Charoen P, Peltonen L, Freimer N, Elliott P, Jarvelin M-R, Schumann Get al., 2011, Glucocorticoid receptor (NR3C1) gene polymorphisms and onset of alcohol abuse in adolescents, ADDICTION BIOLOGY, Vol: 16, Pages: 510-513, ISSN: 1355-6215

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• Citations: 30

Fox ER, Young JH, Li Y, Dreisbach AW, Keating BJ, Musani SK, Liu K, Morrison AC, Ganesh S, Kutlar A, Ramachandran VS, Polak JF, Fabsitz RR, Dries DL, Farlow DN, Redline S, Adeyemo A, Hirschorn JN, Sun YV, Wyatt SB, Penman AD, Palmas W, Rotter JI, Townsend RR, Doumatey AP, Tayo BO, Mosley TH, Lyon HN, Kang SJ, Rotimi CN, Cooper RS, Franceschini N, Curb JD, Martin LW, Eaton CB, Kardia SL, Taylor HA, Caulfield MJ, Ehret GB, Johnson T, International Consortium for Blood Pressure Genome-wide Association Studies ICBP-GWAS, Chakravarti A, Zhu X, Levy Det al., 2011, Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study., Human Molecular Genetics, Vol: 20, Pages: 2273-2284, ISSN: 1460-2083

The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10(-8)) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10(-8)). The top IBC association for SBP was rs2012318 (P= 6.4 × 10(-6)) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10(-6)) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexity.

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Schumann G, Coin LJ, Lourdusamy A, Charoen P, Berger KH, Stacey D, Desrivieres S, Aliev FA, Khan AA, Amin N, Aulchenko YS, Bakalkin G, Bakker SJ, Balkau B, Beulens JW, Bilbao A, de Boer RA, Beury D, Bots ML, Breetvelt EJ, Cauchi S, Cavalcanti-Proenca C, Chambers JC, Clarke T-K, Dahmen N, de Geus EJ, Dick D, Ducci F, Easton A, Edenberg HJ, Esko T, Fernandez-Medarde A, Foroud T, Freimer NB, Girault J-A, Grobbee DE, Guarrera S, Gudbjartsson DF, Hartikainen A-L, Heath AC, Hesselbrock V, Hofman A, Hottenga J-J, Isohanni MK, Kaprio J, Khaw K-T, Kuehnel B, Laitinen J, Lobbens S, Luan J, Mangino M, Maroteaux M, Matullo G, McCarthy MI, Mueller C, Navis G, Numans ME, Nunez A, Nyholt DR, Onland-Moret CN, Oostra BA, O'Reilly PF, Palkovits M, Penninx BW, Polidoro S, Pouta A, Prokopenko I, Ricceri F, Santos E, Smit JH, Soranzo N, Song K, Sovio U, Stumvoll M, Surakk I, Thorgeirsson TE, Thorsteinsdottir U, Troakes C, Tyrfingsson T, Toenjes A, Uiterwaal CS, Uitterlinden AG, van der Harst P, van der Schouw YT, Staehlin O, Vogelzangs N, Vollenweider P, Waeber G, Wareham NJ, Waterworth DM, Whitfield JB, Wichmann EH, Willemsen G, Witteman JC, Yuan X, Zhai G, Zhao JH, Zhang W, Martin NG, Metspalu A, Doering A, Scott J, Spector TD, Loos RJ, Boomsma DI, Mooser V, Peltonen L, Stefansson K, van Duijn CM, Vineis P, Sommer WH, Kooner JS, Spanagel R, Heberlein UA, Jarvelin M-R, Elliott Pet al., 2011, Genome-wide association and genetic functional studies identify <i>autism susceptibility candidate 2</i> gene (AUTS2) in the regulation of alcohol consumption (vol 108, pg 7119, 2011), PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 108, Pages: 9316-9316, ISSN: 0027-8424

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Obeidat M, Wain LV, Shrine N, Kalsheker N, Artigas MS, Repapi E, Burton PR, Johnson T, Ramasamy A, Zhao JH, Zhai G, Huffman JE, Vitart V, Albrecht E, Igl W, Hartikainen A-L, Pouta A, Cadby G, Hui J, Palmer LJ, Hadley D, McArdle WL, Rudnicka AR, Barroso I, Loos RJF, Wareham NJ, Mangino M, Soranzo N, Spector TD, Glaeser S, Homuth G, Voelzke H, Deloukas P, Granell R, Henderson J, Grkovic I, Jankovic S, Zgaga L, Polasek O, Rudan I, Wright AF, Campbell H, Wild SH, Wilson JF, Heinrich J, Imboden M, Probst-Hensch NM, Gyllensten U, Johansson A, Zaboli G, Mustelin L, Rantanen T, Surakka I, Kaprio J, Jarvelin M-R, Hayward C, Evans DM, Koch B, Musk AW, Elliott P, Strachan DP, Tobin MD, Sayers I, Hall IPet al., 2011, A Comprehensive Evaluation of Potential Lung Function Associated Genes in the SpiroMeta General Population Sample, PLOS One, Vol: 6, ISSN: 1932-6203

Rationale: Lung function measures are heritable traits that predict population morbidity and mortality and are essential forthe diagnosis of chronic obstructive pulmonary disease (COPD). Variations in many genes have been reported to affectthese traits, but attempts at replication have provided conflicting results. Recently, we undertook a meta-analysis ofGenome Wide Association Study (GWAS) results for lung function measures in 20,288 individuals from the generalpopulation (the SpiroMeta consortium). Objectives: To comprehensively analyse previously reported genetic associations with lung function measures, and toinvestigate whether single nucleotide polymorphisms (SNPs) in these genomic regions are associated with lung function ina large population sample.Methods: We analysed association for SNPs tagging 130 genes and 48 intergenic regions (+/210 kb), after conducting asystematic review of the literature in the PubMed database for genetic association studies reporting lung functionassociations.Results: The analysis included 16,936 genotyped and imputed SNPs. No loci showed overall significant association for FEV1or FEV1/FVC traits using a carefully defined significance threshold of 1.361025. The most significant loci associated withFEV1 include SNPs tagging MACROD2 (P = 6.8161025), CNTN5 (P = 4.3761024), and TRPV4 (P = 1.5861023). Among eversmokers,SERPINA1 showed the most significant association with FEV1 (P = 8.4161025), followed by PDE4D (P = 1.2261024).The strongest association with FEV1/FVC ratio was observed with ABCC1 (P = 4.3861024), and ESR1 (P = 5.4261024) amongever-smokers.Conclusions: Polymorphisms spanning previously associated lung function genes did not show strong evidence forassociation with lung function measures in the SpiroMet

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Schumann G, Coin LJ, Lourdusamy A, Charoen P, Berger KH, Stacey D, Desrivieres S, Aliev FA, Khan AA, Amin N, Aulchenko YS, Bakalkin G, Bakker SJ, Balkau B, Beulens JW, Bilbao A, de Boer RA, Beury D, Bots ML, Breetvelt EJ, Cauchi S, Cavalcanti-Proenca C, Chambers JC, Clarke T-K, Dahmen N, de Geus EJ, Dick D, Ducci F, Easton A, Edenberg HJ, Esko T, Fernandez-Medarde A, Foroud T, Freimer NB, Girault J-A, Grobbee DE, Guarrera S, Gudbjartsson DF, Hartikainen A-L, Heath AC, Hesselbrock V, Hofman A, Hottenga J-J, Isohanni MK, Kaprio J, Khaw K-T, Kuehnel B, Laitinen J, Lobbens S, Luan J, Mangino M, Maroteaux M, Matullo G, McCarthy MI, Mueller C, Navis G, Numans ME, Nunez A, Nyholt DR, Onland-Moret CN, Oostra BA, O'Reilly PF, Palkovits M, Penninx BW, Polidoro S, Pouta A, Prokopenko I, Ricceri F, Santos E, Smit JH, Soranzo N, Song K, Sovio U, Stumvoll M, Surakk I, Thorgeirsson TE, Thorsteinsdottir U, Troakes C, Tyrfingsson T, Toenjes A, Uiterwaal CS, Uitterlinden AG, van der Harst P, van der Schouw YT, Staehlin O, Vogelzangs N, Vollenweider P, Waeber G, Wareham NJ, Waterworth DM, Whitfield JB, Wichmann EH, Willemsen G, Witteman JC, Yuan X, Zhai G, Zhao JH, Zhang W, Martin NG, Metspalu A, Doering A, Scott J, Spector TD, Loos RJ, Boomsma DI, Mooser V, Peltonen L, Stefansson K, van Duijn CM, Vineis P, Sommer WH, Kooner JS, Spanagel R, Heberlein UA, Jarvelin M-R, Elliott Pet al., 2011, Genome-wide association and genetic functional studies identify <i>autism susceptibility candidate 2</i> gene (<i>AUTS2</i>) in the regulation of alcohol consumption, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 108, Pages: 7119-7124, ISSN: 0027-8424

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• Citations: 208

Ducci F, Kaakinen M, Pouta A, Hartikainen A-L, Veijola J, Isohanni M, Charoen P, Coin L, Hoggart C, Ekelund J, Peltonen L, Freimer N, Elliott P, Schumann G, Jaervelin M-Ret al., 2011, <i>TTC12</i>-<i>ANKK1</i>-<i>DRD2</i> and <i>CHRNA5</i>-<i>CHRNA3</i>-<i>CHRNB4</i> Influence Different Pathways Leading to Smoking Behavior from Adolescence to Mid-Adulthood, BIOLOGICAL PSYCHIATRY, Vol: 69, Pages: 650-660, ISSN: 0006-3223

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• Citations: 58

Brown IJ, Stamler J, Van Horn L, Robertson CE, Chan Q, Dyer AR, Huang C-C, Rodriguez BL, Zhao L, Daviglus ML, Ueshima H, Elliott Pet al., 2011, Sugar-Sweetened Beverage, Sugar Intake of Individuals, and Their Blood Pressure International Study of Macro/Micronutrients and Blood Pressure, HYPERTENSION, Vol: 57, Pages: 695-+, ISSN: 0194-911X

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• Citations: 147

Choquet H, Labrune Y, De Graeve F, Hinney A, Hebebrand J, Scherag A, Lecoeur C, Tauber M, Balkau B, Elliot P, Jarvelin M-R, Walley AJ, Besnard P, Froguel P, Meyre Det al., 2011, Lack of Association of <i>CD36</i> SNPs With Early Onset Obesity: A Meta-Analysis in 9,973 European Subjects, OBESITY, Vol: 19, Pages: 833-839, ISSN: 1930-7381

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• Citations: 17

Kilpelaeinen TO, den Hoed M, Ong KK, Grontved A, Brage S, Jameson K, Cooper C, Khaw K-T, Ekelund U, Wareham NJ, Loos RJFet al., 2011, Obesity-susceptibility loci have a limited influence on birth weight: a meta-analysis of up to 28,219 individuals, AMERICAN JOURNAL OF CLINICAL NUTRITION, Vol: 93, Pages: 851-860, ISSN: 0002-9165

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• Citations: 48

Peden JF, Hopewell JC, Saleheen D, Chambers JC, Hager J, Soranzo N, Collins R, Danesh J, Elliott P, Farrall M, Stirrups K, Zhang W, Hamsten A, Parish S, Lathrop M, Watkins H, Clarke R, Deloukas P, Kooner JS, Goel A, Ongen H, Strawbridge RJ, Heath S, Malarstig A, Helgadottir A, Ohrvik J, Murtaza M, Potter S, Hunt SE, Delepine M, Jalilzadeh S, Axelsson T, Syvanen A-C, Gwilliam R, Bumpstead S, Gray E, Edkins S, Folkersen L, Kyriakou T, Franco-Cereceda A, Gabrielsen A, Seedorf U, Eriksson P, Offer A, Bowman L, Sleight P, Armitage J, Peto R, Abecasis G, Ahmed N, Caulfield M, Donnelly P, Froguel P, Kooner AS, McCarthy MI, Samani NJ, Scott J, Sehmi J, Silveira A, Hellenius M-L, van't Hooft FM, Olsson G, Rust S, Assmann G, Barlera S, Tognoni G, Franzosi MG, Linksted P, Green FR, Rasheed A, Zaidi M, Shah N, Samuel M, Mallick NH, Azhar M, Zaman KS, Samad A, Ishaq M, Gardezi AR, Memon F-U-R, Frossard PM, Spector T, Peltonen L, Nieminen MS, Sinisalo J, Salomaa V, Ripatti S, Bennett D, Leander K, Gigante B, de Faire U, Pietri S, Gori F, Marchioli R, Sivapalaratnam S, Kastelein JJP, Trip MD, Theodoraki EV, Dedoussis GV, Engert JC, Yusuf S, Anand SSet al., 2011, A genome-wide association study in Europeans and South Asians identifies five new loci for coronary artery disease, NATURE GENETICS, Vol: 43, Pages: 339-U89, ISSN: 1061-4036

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• Citations: 532

Speliotes EK, Yerges-Armstrong LM, Wu J, Hernaez R, Kim LJ, Palmer CD, Gudnason V, Eiriksdottir G, Garcia ME, Launer LJ, Nalls MA, Clark JM, Mitchell BD, Shuldiner AR, Butler JL, Tomas M, Hoffmann U, Hwang SJ, Massaro JM, O'Donnell CJ, Sahani DV, Salomaa V, Schadt EE, Schwartz SM, Siscovick DS, Voight BF, Carr JJ, Feitosa MF, Harris TB, Fox CS, Smith AV, Kao WH, Hirschhorn JN, Borecki IBet al., 2011, Genome-wide association analysis identifies variants associated with nonalcoholic fatty liver disease that have distinct effects on metabolic traits, PLOS Genetics, Vol: 7, ISSN: 1553-7390

Nonalcoholic fatty liver disease (NAFLD) clusters in families, but the only known common genetic variants influencing risk are near PNPLA3. We sought to identify additional genetic variants influencing NAFLD using genome-wide association (GWA) analysis of computed tomography (CT) measured hepatic steatosis, a non-invasive measure of NAFLD, in large population based samples. Using variance components methods, we show that CT hepatic steatosis is heritable ( approximately 26%-27%) in family-based Amish, Family Heart, and Framingham Heart Studies (n = 880 to 3,070). By carrying out a fixed-effects meta-analysis of genome-wide association (GWA) results between CT hepatic steatosis and approximately 2.4 million imputed or genotyped SNPs in 7,176 individuals from the Old Order Amish, Age, Gene/Environment Susceptibility-Reykjavik study (AGES), Family Heart, and Framingham Heart Studies, we identify variants associated at genome-wide significant levels (p<5x10(-8)) in or near PNPLA3, NCAN, and PPP1R3B. We genotype these and 42 other top CT hepatic steatosis-associated SNPs in 592 subjects with biopsy-proven NAFLD from the NASH Clinical Research Network (NASH CRN). In comparisons with 1,405 healthy controls from the Myocardial Genetics Consortium (MIGen), we observe significant associations with histologic NAFLD at variants in or near NCAN, GCKR, LYPLAL1, and PNPLA3, but not PPP1R3B. Variants at these five loci exhibit distinct patterns of association with serum lipids, as well as glycemic and anthropometric traits. We identify common genetic variants influencing CT-assessed steatosis and risk of NAFLD. Hepatic steatosis associated variants are not uniformly associated with NASH/fibrosis or result in abnormalities in serum lipids or glycemic and anthropometric traits, suggesting genetic heterogeneity in the pathways influencing these traits.

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Dehghan A, Dupuis J, Barbalic M, Bis JC, Eiriksdottir G, Lu C, Pellikka N, Wallaschofski H, Kettunen J, Henneman P, Baumert J, Strachan DP, Fuchsberger C, Vitart V, Wilson JF, Pare G, Naitza S, Rudock ME, Surakka I, de Geus EJC, Alizadeh BZ, Guralnik J, Shuldiner A, Tanaka T, Zee RYL, Schnabel RB, Nambi V, Kavousi M, Ripatti S, Nauck M, Smith NL, Smith AV, Sundvall J, Scheet P, Liu Y, Ruokonen A, Rose LM, Larson MG, Hoogeveen RC, Freimer NB, Teumer A, Tracy RP, Launer LJ, Buring JE, Yamamoto JF, Folsom AR, Sijbrands EJG, Pankow J, Elliott P, Keaney JF, Sun W, Sarin A-P, Fontes JD, Badola S, Astor BC, Hofman A, Pouta A, Werdan K, Greiser KH, Kuss O, Schwabedissen HEMZ, Thiery J, Jamshidi Y, Nolte IM, Soranzo N, Spector TD, Voelzke H, Parker AN, Aspelund T, Bates D, Young L, Tsui K, Siscovick DS, Guo X, Rotter JI, Uda M, Schlessinger D, Rudan I, Hicks AA, Penninx BW, Thorand B, Gieger C, Coresh J, Willemsen G, Harris TB, Uitterlinden AG, Jaervelin M-R, Rice K, Radke D, Salomaa V, van Dijk KW, Boerwinkle E, Vasan RS, Ferrucci L, Gibson QD, Bandinelli S, Snieder H, Boomsma DI, Xiao X, Campbell H, Hayward C, Pramstaller PP, van Duijn CM, Peltonen L, Psaty BM, Gudnason V, Ridker PM, Homuth G, Koenig W, Ballantyne CM, Witteman JCM, Benjamin EJ, Perola M, Chasman DIet al., 2011, Meta-Analysis of Genome-Wide Association Studies in &gt;80 000 Subjects Identifies Multiple Loci for C-Reactive Protein Levels, CIRCULATION, Vol: 123, Pages: 731-U151, ISSN: 0009-7322

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• Citations: 404

Wensley F, Gao P, Burgess S, Kaptoge S, Di Angelantonio E, Shah T, Engert JC, Clarke R, Davey-Smith G, Nordestgaard BG, Saleheen D, Samani NJ, Sandhu M, Anand S, Pepys MB, Smeeth L, Whittaker J, Casas JP, Thompson SG, Hingorani AD, Danesh J, Eiriksdottir G, Harris TB, Launer LJ, Gudnason V, Folsom AR, Andrews G, Ballantyne CM, Samani NJ, Hall AS, Braund PS, Balmforth AJ, Whincup PH, Morris R, Lawlor DA, Lowe GDO, Timpson N, Ebrahim S, Ben-Shlomo Y, Davey-Smith G, Timpson N, Nordestgaard BG, Tybjaerg-Hansen A, Zacho J, Brown M, Sandhu M, Ricketts SL, Ashford S, Lange L, Reiner A, Cushman M, Tracy R, Wu C, Ge J, Zou Y, Sun A, Hung J, McQuillan B, Thompson P, Beilby J, Warrington N, Palmer LJ, Wanner C, Drechsler C, Hoffmann MM, Fowkes FGR, Lowe GDO, Tzoulaki I, Kumari M, Miller M, Marmot M, Onland-Moret C, van der Schouw YT, Boer JM, Wijmenga C, Ricketts SL, Ashford S, Sandhu M, Khaw K-T, Vasan RS, Schnabel RB, Yamamoto JF, Benjamin EJ, Schunkert H, Erdmann J, Koenig IR, Hengstenberg C, Chiodini B, Franzosi MG, Pietri S, Gori F, Rudock M, Liu Y, Lohman K, Harris TB, Humphries SE, Hamsten A, Norman PE, Hankey GJ, Jamrozik K, Palmer LJ, Rimm EB, Pai JK, Psaty BM, Heckbert SR, Bis JC, Yusuf S, Anand S, Engert JC, Xie C, Collins R, Clarke R, Bennett D, Kooner J, Chambers J, Elliott P, Maerz W, Kleber ME, Boehm BO, Winkelmann BR, Melander O, Berglund G, Koenig W, Thorand B, Baumert J, Peters A, Rimm EB, Manson J, Pai JK, Humphries SE, Cooper JA, Talmud PJ, Ladenvall P, Johansson L, Jansson J-H, Hallmans G, Reilly MP, Qu L, Li M, Rader DJ, Watkins H, Clarke R, Hopewell J, Saleheen D, Danesh J, Frossard P, Sattar N, Robertson M, Shepherd J, Schaefer E, Hofman A, Witteman JCM, Kardys I, Dehghan A, de Faire U, Bennet A, Gigante B, Leander K, Ben-Shlomo Y, Davey-Smith G, Timpson N, Peters B, Maitland-van der Zee AH, de Boer A, Klungel O, Reiner A, Manson J, Greenland P, Dai J, Liu S, Kumari M, Brunner E, Kivimaki M, Marmot M, Sattar N, O'Reilly D, Ford I, Packard CJet al., 2011, Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data, British Medical Journal, Vol: 342, ISSN: 1468-5833

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

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Finucane MM, Stevens GA, Cowan MJ, Danaei G, Lin JK, Paciorek CJ, Singh GM, Gutierrez HR, Lu Y, Bahalim AN, Farzadfar F, Riley LM, Ezzati Met al., 2011, National, regional, and global trends in body-mass index since 1980: systematic analysis of health examination surveys and epidemiological studies with 960 country-years and 9.1 million participants, LANCET, Vol: 377, Pages: 557-567, ISSN: 0140-6736

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• Citations: 3005

Danaei G, Finucane MM, Lin JK, Singh GM, Paciorek CJ, Cowan MJ, Farzadfar F, Stevens GA, Lim SS, Riley LM, Ezzati M, Abdeen Z, Agyemang C, Al Nsour M, Ali MM, Ambady R, Babu BV, Barbagallo CM, Barcelo A, Barreto SM, Barros H, Bautista LE, Bjerregaard P, Bjoerkelund C, Bo S, Bobak M, Bonora E, Botana MA, Bovet P, Breckenkamp J, Breteler MM, Broda G, Brown IJ, Bursztyn M, de Leon AC, Casiglia E, Castetbon K, Chatterji S, Chen Z, Chen C-J, Chua L, Cifkova R, Cobiac LJ, Cooper RS, Dankner RS, Dong G-H, Elliott P, Erem C, Esteghamati A, Fan J-G, Ferreccio C, Firmo JO, Fornes NS, Fuchs FD, Getz L, Giampaoli S, Gomez LF, Graff-Iversen S, Carvajal RG, Gulliford MC, Gupta PC, Gureje O, Hansen TW, He J, Heinrich J, Hennis A, Herrera VM, Ho SC, Ibrahim MM, Ikeda N, Jafar TH, Joffres MR, Jonas JB, Kamadjeu RM, Karalis I, Kastarinen MJ, Katz J, Kelly P, Khalilzadeh O, Khang Y-H, Kiechl S, Kim KW, Kobayashi J, Kubinova R, Kusuma YS, Lam TH, Lawes CMM, Le C, Lee J, Lin X, Lin H-H, Lin C-C, Liu X, Lorbeer R, Ma S, Ma G, Magliano DJ, Makdisse M, Mancia G, Mbanya JCN, Miettola J, Minh HV, Miranda JJ, Mohamed MK, Mohan V, Mokdad AH, Morales DD, Morgan K, Muiesan LM, Muntoni S, Nabipour I, Nangia V, Neuhauser H, Ninomiya T, Olivieri O, Oenal AE, Onat A, Orostegui M, Panagiotakos DB, Panza F, Pednekar MS, Perez C, Perez-Fernandez R, Pichardo R, Phua HP, Plans P, Poulter N, Raitakari OT, Rampal S, Rampal L, Redon J, Revilla L, Roaeid RB, Rojas-Martinez R, Sanisoglu SY, Sans S, Schelleman H, Schneider IJC, Silva DAS, Silva E, Simons LA, Smith M, Soebardi S, Solfrizzi V, Stein AD, Stergiou GS, Stessman J, Suka M, Tambs K, Tesfaye F, Thorogood M, Tilvis RS, Trenkwalder P, Tuomilehto JO, Tzourio C, Vander Hoorn S, Vanderpump MP, Verschuren M, Vioque J, Waspadji S, Wilhelmsen L, Willeit J, Woodward M, Xavier AJ, Xu L, Yang G, Yeh L-C, Yoon J-S, You Q, Zhou Met al., 2011, National, regional, and global trends in systolic blood pressure since 1980: systematic analysis of health examination surveys and epidemiological studies with 786 country-years and 5.4 million participants, LANCET, Vol: 377, Pages: 568-577, ISSN: 0140-6736

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• Citations: 713

Iszatt N, Nieuwenhuijsen MJ, Nelson P, Elliott P, Toledano MBet al., 2011, Water Consumption and Use, Trihalomethane Exposure, and the Risk of Hypospadias, PEDIATRICS, Vol: 127, Pages: E389-E397, ISSN: 0031-4005

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• Citations: 24

Curb JD, Ueshima H, Rodriguez BL, He Q, Koropatnick TA, Nakagawa H, Sakata K, Saitoh S, Okayama Aet al., 2011, Differences in lipoprotein particle subclass distribution for Japanese Americans in Hawaii and Japanese in Japan: The INTERLIPID Study, JOURNAL OF CLINICAL LIPIDOLOGY, Vol: 5, Pages: 30-36, ISSN: 1933-2874

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• Citations: 4

Schuz J, Elliott P, Auvinen A, Kromhout H, Poulsen AH, Johansen C, Olsen JH, Hillert L, Feychting M, Fremling K, Toledano M, Heinavaara S, Slottje P, Vermeulen R, Ahlbom Aet al., 2011, An international prospective cohort study of mobile phone users and health (Cosmos): Design considerations and enrolment, CANCER EPIDEMIOLOGY, Vol: 35, Pages: 37-43, ISSN: 1877-7821

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• Citations: 53

Sakurai M, Stamler J, Miura K, Brown IJ, Nakagawa H, Elliott P, Ueshima H, Chan Q, Tzoulaki I, Dyer AR, Okayama A, Zhao Let al., 2011, Relationship of dietary cholesterol to blood pressure: the INTERMAP study, JOURNAL OF HYPERTENSION, Vol: 29, Pages: 222-228, ISSN: 0263-6352

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• Citations: 39

Toledano MB, Bennett JE, Hambly P, de Hoogh K, Elliott P, Nieuwenhuijsen MJet al., 2011, Chlorination Disinfection By-products and Risk of Stillbirths in England and Wales, Joint Conference of International-Society-of-Exposure-Science/International-Society-for-Environmental-Epidemiology, Publisher: LIPPINCOTT WILLIAMS & WILKINS, Pages: S126-S126, ISSN: 1044-3983

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Elliott P, Toledano MB, Bennett JE, Beale L, de Hoogh K, Best N, Briggs DJet al., 2011, Case-control Study of Mobile Phone Base Stations and Early Childhood Cancers, Joint Conference of International-Society-of-Exposure-Science/International-Society-for-Environmental-Epidemiology, Publisher: LIPPINCOTT WILLIAMS & WILKINS, Pages: S52-S53, ISSN: 1044-3983

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• Citations: 1

Jacquemont S, Reymond A, Zufferey F, Harewood L, Walters RG, Kutalik Z, Martinet D, Shen Y, Valsesia A, Beckmann ND, Thorleifsson G, Belfiore M, Bouquillon S, Campion D, de Leeuw N, de Vries BB, Esko T, Fernandez BA, Fernandez-Aranda F, Fernandez-Real JM, Gratacos M, Guilmatre A, Hoyer J, Jarvelin MR, Kooy RF, Kurg A, Le Caignec C, Mannik K, Platt OS, Sanlaville D, Van Haelst MM, Villatoro Gomez S, Walha F, Wu BL, Yu Y, Aboura A, Addor MC, Alembik Y, Antonarakis SE, Arveiler B, Barth M, Bednarek N, Bena F, Bergmann S, Beri M, Bernardini L, Blaumeiser B, Bonneau D, Bottani A, Boute O, Brunner HG, Cailley D, Callier P, Chiesa J, Chrast J, Coin L, Coutton C, Cuisset JM, Cuvellier JC, David A, de Freminville B, Delobel B, Delrue MA, Demeer B, Descamps D, Didelot G, Dieterich K, Disciglio V, Doco-Fenzy M, Drunat S, Duban-Bedu B, Dubourg C, El-Sayed Moustafa JS, Elliott P, Faas BH, Faivre L, Faudet A, Fellmann F, Ferrarini A, Fisher R, Flori E, Forer L, Gaillard D, Gerard M, Gieger C, Gimelli S, Gimelli G, Grabe HJ, Guichet A, Guillin O, Hartikainen AL, Heron D, Hippolyte L, Holder M, Homuth G, Isidor B, Jaillard S, Jaros Z, Jimenez-Murcia S, Helas GJet al., 2011, Mirror extreme BMI phenotypes associated with gene dosage at the chromosome 16p11.2 locus, Nature, Vol: 478, Pages: 97-102, ISSN: 1476-4687

Both obesity and being underweight have been associated with increased mortality. Underweight, defined as a body mass index (BMI) </= 18.5 kg per m(2) in adults and </= -2 standard deviations from the mean in children, is the main sign of a series of heterogeneous clinical conditions including failure to thrive, feeding and eating disorder and/or anorexia nervosa. In contrast to obesity, few genetic variants underlying these clinical conditions have been reported. We previously showed that hemizygosity of a approximately 600-kilobase (kb) region on the short arm of chromosome 16 causes a highly penetrant form of obesity that is often associated with hyperphagia and intellectual disabilities. Here we show that the corresponding reciprocal duplication is associated with being underweight. We identified 138 duplication carriers (including 132 novel cases and 108 unrelated carriers) from individuals clinically referred for developmental or intellectual disabilities (DD/ID) or psychiatric disorders, or recruited from population-based cohorts. These carriers show significantly reduced postnatal weight and BMI. Half of the boys younger than five years are underweight with a probable diagnosis of failure to thrive, whereas adult duplication carriers have an 8.3-fold increased risk of being clinically underweight. We observe a trend towards increased severity in males, as well as a depletion of male carriers among non-medically ascertained cases. These features are associated with an unusually high frequency of selective and restrictive eating behaviours and a significant reduction in head circumference. Each of the observed phenotypes is the converse of one reported in carriers of deletions at this locus. The phenotypes correlate with changes in transcript levels for genes mapping within the duplication but not in flanking regions. The reciprocal impact of these 16p11.2 copy-number variants indicates that severe obesity and being underweight could have mirror aetiolog

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Yap IKS, Brown IJ, Chan Q, Wijeyesekera A, Garcia-Perez I, Bictash M, Loo RL, Chadeau-Hyam M, Ebbeis T, De Iorio M, Maibaum E, Zhao L, Kesteloot H, Daviglus ML, Stamler J, Nicholson JK, Elliott P, Holmes Eet al., 2010, Metabolome-Wide Association Study Identifies Multiple Biomarkers that Discriminate North and South Chinese Populations at Differing Risks of Cardiovascular Disease INTERMAP Study, JOURNAL OF PROTEOME RESEARCH, Vol: 9, Pages: 6647-6654, ISSN: 1535-3893

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• Citations: 94

Hopewell JC, Peden J, Saleheen D, Chambers J, Clarke R, Collins R, Danesh J, Deloukas P, Elliott P, Farrall M, Hager J, Hamsten A, Kooner J, Lathrop M, Parish S, Watkins Het al., 2010, A Genome-Wide Association Study of Risk of Coronary Artery Disease in European and South Asian Populations, CIRCULATION, Vol: 122, ISSN: 0009-7322

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Brown IJ, Elliott P, 2010, Recent findings from Mendelian randomization studies of cardiovascular disease, Current Cardiovascular Risk Reports, Vol: 4, Pages: 429-436

Judgments as to causality of associations between risk factors and disease involve a weighing of the available evidence from animal and human studies. The human data include observational studies, results of which may be confounded, and randomized trials, which may be unavailable or infeasible, thus limiting the ability to make causal inference. Mendelian randomization offers an additional approach to help assess causality. The concept relies on the random assignment of alleles at meiosis as the basis for a natural randomized experiment linking genetic variants to intermediate risk factors and disease. Recent Mendelian randomization studies have provided evidence for a causal role of serum lipoprotein(a) in coronary heart disease, and against a causal role for plasma C-reactive protein. Although a valid Mendelian randomization experiment is subject to a number of assumptions and limitations, it is a useful adjunct to assess causality, especially when randomized trials are unavailable.

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Tabara Y, Kohara K, Kita Y, Hirawa N, Katsuya T, Ohkubo T, Hiura Y, Tajima A, Morisaki T, Miyata T, Nakayama T, Takashima N, Nakura J, Kawamoto R, Takahashi N, Hata A, Soma M, Imai Y, Kokubo Y, Okamura T, Tomoike H, Iwai N, Ogihara T, Inoue I, Tokunaga K, Johnson T, Caulfield M, Munroe P, Umemura S, Ueshima H, Miki Tet al., 2010, Common Variants in the ATP2B1 Gene Are Associated With Susceptibility to Hypertension The Japanese Millennium Genome Project, HYPERTENSION, Vol: 56, Pages: 973-U533, ISSN: 0194-911X

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• Citations: 80

Waterworth DM, Ricketts SL, Song K, Chen L, Zhao JH, Ripatti S, Aulchenko YS, Zhang W, Yuan X, Lim N, Luan J, Ashford S, Wheeler E, Young EH, Hadley D, Thompson JR, Braund PS, Johnson T, Struchalin M, Surakka I, Luben R, Khaw K-T, Rodwell SA, Loos RJF, Boekholdt SM, Inouye M, Deloukas P, Elliott P, Schlessinger D, Sanna S, Scuteri A, Jackson A, Mohlke KL, Tuomilehto J, Roberts R, Stewart A, Kesaeniemi YA, Mahley RW, Grundy SM, McArdle W, Cardon L, Waeber G, Vollenweider P, Chambers JC, Boehnke M, Abecasis GR, Salomaa V, Jaervelin M-R, Ruokonen A, Barroso I, Epstein SE, Hakonarson HH, Rader DJ, Reilly MP, Witteman JCM, Hall AS, Samani NJ, Strachan DP, Barter P, van Duijn CM, Kooner JS, Peltonen L, Wareham NJ, McPherson R, Mooser V, Sandhu MSet al., 2010, Genetic Variants Influencing Circulating Lipid Levels and Risk of Coronary Artery Disease, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 30, Pages: 2264-U566, ISSN: 1079-5642

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• Citations: 319