University Lecturer in Cardiovascular Epidemiology
Tel: +44 (0) 1223 748673
Genetic discovery: Adam’s main interests revolve around the identification of genetic variation linked with coronary disease and related phenotypes (eg, vascular risk factors such as lipids) using customised SNP arrays. Current efforts in this area include the 50,000-participant CardioMetabochip+ consortium and the 100,000 participant Exome+ consortium that are coordinated at CEU.
Human genetics to inform therapeutics: By relating informative genetic variants (eg, variants of known function) to disease outcomes and phenotypes, inference about the likely efficacy and safety profile of therapeutic agents (or potential therapeutic agents) can be made. For example, the work of Adam and colleagues at CEU has highlighted the relationship of IL6R variants to risk of heart disease, raising the possibility of monoclonal antibodies being repurposed from inflammatory conditions to cardiovascular pathways. Adam works closely with large pharmaceutical companies to help discover and evaluate pathways of potential therapeutic interest.
EPIC-CVD: Adam is the Scientific Coordinator of the EPIC-Heart/EPIC-CVD study, which is a pan-European study of incident coronary disease and stroke including participants from 23 centres across 10 European countries. This project has a wealth of genetic, biochemical and risk factor data, which are predominantly utilised for the study of gene-environment interaction, cardiovascular risk prediction, and genetic discovery.
Following training in Genetics at the University of Cambridge and Genetic Epidemiology at the University of Sheffield, Adam completed a PhD in meta-analysis of genetic association studies of coronary heart disease at the University of Cambridge. This research was carried out jointly with the PHG Foundation, the MRC Biostatistics Unit, and the Cardiovascular Epidemiology Unit.
Since his PhD, Adam has worked in the Cardiovascular Epidemiology Unit, initially as a post-doctoral Research Associate, and since 2012 as a University Lecturer in Cardiovascular Epidemiology. As well as leading a Genetic Epidemiology team, Adam also overseas the Unit’s PhD students.
Adam sits on the Admissions Committe and the Management Committee for the MPhil courses in Epidemiology and Public Health, as well as leading the Research Synthesis Module taught in term 1. In addition, Adam lectures in the Chronic Disease Epidemiology module, as well as lecturing on Research Synthesis and Genetic Epidemiology on the TMAT course.
Adam is the CEU’s PhD student coordinator and also coordinates the quantitative stream of the BHF 1+3 PhD programme in Cardiovascular Research.
Adam currently supervises 1 MPhil student and 3 PhD students.
Mendelian randomization analysis with multiple genetic variants using summarized data. Burgess S, Butterworth A, Thompson SG. Genet Epidemiol. 2013;37(7):658-65.
Inflammatory cytokines and risk of coronary heart disease: new prospective study and updated meta-analysis. Kaptoge S, Seshasai SR, Gao P, Freitag DF, Butterworth AS, Borglykke A, Di Angelantonio E, Gudnason V, Rumley A, Lowe GD, Jørgensen T, Danesh J. Eur Heart J. 2013. [Epub ahead of print]
Functional IL6R 358Ala allele impairs classical IL-6 receptor signaling and influences risk of diverse inflammatory diseases. Ferreira RC, Freitag DF, Cutler AJ, Howson JM, Rainbow DB, Smyth DJ, Kaptoge S, Clarke P, Boreham C, Coulson RM, Pekalski ML, Chen WM, Onengut-Gumuscu S, Rich SS, Butterworth AS, Malarstig A, Danesh J, Todd JA. PLoS Genet. 2013;9(4):e1003444.
Use of Mendelian randomisation to assess potential benefit of clinical intervention. Burgess S, Butterworth A, Malarstig A, Thompson SG. BMJ. 2012;345:e7325.
C-reactive protein, fibrinogen, and cardiovascular disease prediction. Emerging Risk Factors Collaboration. N Engl J Med. 2012;367(14):1310-20.
Clinical utility of genetic variants for cardiovascular risk prediction: a futile exercise or insufficient data? Di Angelantonio E, Butterworth AS.Circ Cardiovasc Genet. 2012;5(4):387-90.
Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies. Sarwar N*, Butterworth AS*, Freitag DF, Gregson J, Willeit P, Gorman DN, Gao P, Saleheen D, Rendon A, Nelson CP, Braund PS, Hall AS, Chasman DI, Tybjærg-Hansen A, Chambers JC, Benjamin EJ, Franks PW, Clarke R, Wilde AA, Trip MD, Steri M, Witteman JC, Qi L, van der Schoot CE, de Faire U, Erdmann J, Stringham HM, Koenig W, Rader DJ, Melzer D, Reich D, Psaty BM, Kleber ME, Panagiotakos DB, Willeit J, Wennberg P, Woodward M, Adamovic S, Rimm EB, Meade TW, Gillum RF, Shaffer JA, Hofman A, Onat A, Sundström J, Wassertheil-Smoller S, Mellström D, Gallacher J, Cushman M, Tracy RP, Kauhanen J, Karlsson M, Salonen JT, Wilhelmsen L, Amouyel P, Cantin B, Best LG, Ben-Shlomo Y, Manson JE, Davey-Smith G, de Bakker PI, O’Donnell CJ, Wilson JF, Wilson AG, Assimes TL, Jansson JO, Ohlsson C, Tivesten Å, Ljunggren Ö, Reilly MP, Hamsten A, Ingelsson E, Cambien F, Hung J, Thomas GN, Boehnke M, Schunkert H, Asselbergs FW, Kastelein JJ, Gudnason V, Salomaa V, Harris TB, Kooner JS, Allin KH, Nordestgaard BG, Hopewell JC, Goodall AH, Ridker PM, Hólm H, Watkins H, Ouwehand WH, Samani NJ, Kaptoge S, Di Angelantonio E, Harari O, Danesh J. Lancet. 2012;379(9822):1205-13.
Large-scale gene-centric analysis identifies novel variants for coronary artery disease. IBC 50K CAD Consortium, Butterworth AS et al. PLoS Genet. 2011;7(9):e1002260.