Authors

Ron Do, Massachusetts General Hospital
Cristen J. Willer, University of Michigan Medical School
Ellen M. Schmidt, University of Michigan, Ann Arbor
Sebanti Sengupta, University of Michigan, Ann Arbor
Chi Gao, Massachusetts General Hospital
Gina M. Peloso, Massachusetts General Hospital
Stefan Gustafsson, Uppsala Universitet
Stavroula Kanoni, Wellcome Sanger Institute
Andrea Ganna, Uppsala Universitet
Jin Chen, University of Michigan, Ann Arbor
Martin L. Buchkovich, UNC School of Medicine
Samia Mora, Brigham and Women's Hospital
Jacques S. Beckmann, Centre Hospitalier Universitaire Vaudois
Jennifer L. Bragg-Gresham, University of Michigan, Ann Arbor
Hsing Yi Chang, National Health Research Institutes Taiwan
Ayse Demirkan, Erasmus MC
Heleen M. Den Hertog, Erasmus MC
Louise A. Donnelly, University of Dundee School of Medicine
Georg B. Ehret, Hôpitaux Universitaires de Genève
Tõnu Esko, Broad Institute
Mary F. Feitosa, Washington University School of Medicine in St. Louis
Teresa Ferreira, The Wellcome Centre for Human Genetics
Krista Fischer, Tartu Ülikooli Genoomika Instituut
Pierre Fontanillas, Broad Institute
Ross M. Fraser, The University of Edinburgh
Daniel F. Freitag, University of Cambridge
Deepti Gurdasani, Wellcome Sanger Institute
Kauko Heikkilä, Helsingin Yliopisto
Elina Hyppönen, UCL Great Ormond Street Institute of Child Health
Aaron Isaacs, Erasmus MC
Anne U. Jackson, University of Michigan, Ann Arbor
Åsa Johansson, Uppsala Universitet
Toby Johnson, Barts and The London School of Medicine and Dentistry

Document Type

Letter to the Editor

Publication Date

11-1-2013

Abstract

Triglycerides are transported in plasma by specific triglyceride-rich lipoproteins; in epidemiological studies, increased triglyceride levels correlate with higher risk for coronary artery disease (CAD). However, it is unclear whether this association reflects causal processes. We used 185 common variants recently mapped for plasma lipids (P < 5 × 10 -8 for each) to examine the role of triglycerides in risk for CAD. First, we highlight loci associated with both low-density lipoprotein cholesterol (LDL-C) and triglyceride levels, and we show that the direction and magnitude of the associations with both traits are factors in determining CAD risk. Second, we consider loci with only a strong association with triglycerides and show that these loci are also associated with CAD. Finally, in a model accounting for effects on LDL-C and/or high-density lipoprotein cholesterol (HDL-C) levels, the strength of a polymorphism's effect on triglyceride levels is correlated with the magnitude of its effect on CAD risk. These results suggest that triglyceride-rich lipoproteins causally influence risk for CAD. © 2013 Nature America, Inc. All rights reserved.

Publication Source (Journal or Book title)

Nature Genetics

First Page

1345

Last Page

1353

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