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Saleheen D, Zhao W, Young R, Nelson CP, Ho W, Ferguson JF, Rasheed A, Ou K, Nurnberg ST, Bauer RC, Goel A, Do R, Stewart AFR, Hartiala J, Zhang W, Thorleifsson G, Strawbridge RJ, Sinisalo J, Kanoni S, Sedaghat S, Marouli E, Kristiansson K, Hua Zhao J, Scott R, Gauguier D, Shah SH, Smith AV, van Zuydam N, Cox AJ, Willenborg C, Kessler T, Zeng L, Province MA, Ganna A, Lind L, Pedersen NL, White CC, Joensuu A, Edi Kleber M, Hall AS, März W, Salomaa V, O'Donnell C, Ingelsson E, Feitosa MF, Erdmann J, Bowden DW, Palmer CNA, Gudnason V, Faire U, Zalloua P, Wareham N, Thompson JR, Kuulasmaa K, Dedoussis G, Perola M, Dehghan A, Chambers JC, Kooner J, Allayee H, Deloukas P, McPherson R, Stefansson K, Schunkert H, Kathiresan S, Farrall M, Marcel Frossard P, Rader DJ, Samani NJ, Reilly MP
Circulation 135 (24) 2336-2353 [2017-06-13; online 2017-05-01]
Common diseases such as coronary heart disease (CHD) are complex in etiology. The interaction of genetic susceptibility with lifestyle factors may play a prominent role. However, gene-lifestyle interactions for CHD have been difficult to identify. Here, we investigate interaction of smoking behavior, a potent lifestyle factor, with genotypes that have been shown to associate with CHD risk. We analyzed data on 60 919 CHD cases and 80 243 controls from 29 studies for gene-smoking interactions for genetic variants at 45 loci previously reported to be associated with CHD risk. We also studied 5 loci associated with smoking behavior. Study-specific gene-smoking interaction effects were calculated and pooled using fixed-effects meta-analyses. Interaction analyses were declared to be significant at a We identified novel gene-smoking interaction for a variant upstream of the
PubMed 28461624
DOI 10.1161/CIRCULATIONAHA.116.022069
Crossref 10.1161/CIRCULATIONAHA.116.022069
pii: CIRCULATIONAHA.116.022069
pmc: PMC5612779
mid: NIHMS870560