Genetically determined plasma lipid levels and risk of diabetic retinopathy: A mendelian randomization study

Lucia Sobrin, Yong He Chong, Qiao Fan, Alfred Gan, Lynn K. Stanwyck, Georgia Kaidonis, Jamie E. Craig, Jihye Kim, Wen Ling Liao, Yu Chuen Huang, Wen Jane Lee, Yi Jen Hung, Xiuqing Guo, Yang Hai, Eli Ipp, Samuela Pollack, Heather Hancock, Alkes Price, Alan Penman, Paul MitchellGerald Liew, Albert V. Smith, Vilmundur Gudnason, Gavin Tan, Barbara E.K. Klein, Jane Kuo, Xiaohui Li, Mark W. Christiansen, Bruce M. Psaty, Kevin Sandow, Richard A. Jensen, Ronald Klein, Mary Frances Cotch, Jie Jin Wang, Yucheng Jia, Ching J. Chen, Yii Der Ida Chen, Jerome I. Rotter, Fuu Jen Tsai, Craig L. Hanis, Kathryn P. Burdon, Tien Yin Wong, Ching Yu Cheng

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Results from observational studies examining dyslipidemia as a risk factor for diabetic retinopathy (DR) have been inconsistent. We evaluated the causal relationship between plasma lipids and DR using a Mendelian randomization approach. We pooled genome-wide association studies summary statistics from 18 studies for two DR phenotypes: Any DR (N = 2,969 case and 4,096 control subjects) and severe DR (N = 1,277 case and 3,980 control subjects). Previously identified lipid-associated single nucleotide polymorphisms served as instrumental variables. Meta-analysis to combine the Mendelian randomization estimates from different cohorts was conducted. There was no statistically significant change in odds ratios of having any DR or severe DR for any of the lipid fractions in the primary analysis that used single nucleotide polymorphisms that did not have a pleiotropic effect on another lipid fraction. Similarly, there was no significant association in the Caucasian and Chinese subgroup analyses. This study did not show evidence of a causal role of the four lipid fractions on DR. However, the study had limited power to detect odds ratios less than 1.23 per SD in genetically induced increase in plasma lipid levels, thus we cannot exclude that causal relationships with more modest effect sizes exist.

Original languageEnglish
Pages (from-to)3130-3141
Number of pages12
Issue number12
StatePublished - 1 Dec 2017
Externally publishedYes


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