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00925njm 22002777a 4500 dc Ibáñez-Sanz, Gemma author Díez-Villanueva, Anna author Riera-Ponsati, Marina author Fernández-Villa, Tania author Fernandez-Navarro, Pablo L author Bustamante, Mariona author Llorca, Javier author Amiano, Pilar author Ascunce, Nieves author Fernández-Tardón, Guillermo author Salcedo Bellido, Inmaculada author Salas, Dolores author Capelo Álvarez, Rocío author Crous-Bou, Marta author Ortega-Valín, Luis author Perez-Gomez, Beatriz author Castaño-Vinyals, Gemma author Palazuelos, Camilo author Altzibar, Jone M author Ardanaz, Eva author Tardón, Adonina author Jimenez-Moleon, Jose J. author Olmos Juste, Valle author Aragones, Nuria author Pollan-Santamaria, Marina author Kogevinas, Manolis author Moreno, Victor author 2019-09-16 Dyslipidemia and statin use have been associated with colorectal cancer (CRC), but prospective studies have shown mixed results. We aimed to determine whether dyslipidemia is causally linked to CRC risk using a Mendelian randomization approach and to explore the association of statins with CRC. A case-control study was performed including 1336 CRC cases and 2744 controls (MCC-Spain). Subjects were administered an epidemiological questionnaire and were genotyped with an array which included polymorphisms associated with blood lipids levels, selected to avoid pleiotropy. Four genetic lipid scores specific for triglycerides (TG), high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL), or total cholesterol (TC) were created as the count of risk alleles. The genetic lipid scores were not associated with CRC. The ORs per 10 risk alleles, were for TG 0.91 (95%CI: 0.72-1.16, p = 0.44), for HDL 1.14 (95%CI: 0.95-1.37, p = 0.16), for LDL 0.97 (95%CI: 0.81-1.16, p = 0.73), and for TC 0.98 (95%CI: 0.84-1.17, p = 0.88). The LDL and TC genetic risk scores were associated with statin use, but not the HDL or TG. Statin use, overall, was a non-significant protective factor for CRC (OR 0.84; 95%CI: 0.70-1.01, p = 0.060), but lipophilic statins were associated with a CRC risk reduction (OR 0.78; 95%CI 0.66-0.96, p = 0.018). Using the Mendelian randomization approach, our study does not support the hypothesis that lipid levels are associated with the risk of CRC. This study does not rule out, however, a possible protective effect of statins in CRC by a mechanism unrelated to lipid levels. Sci Rep. 2019 Sep 16;9(1):13407. 2045-2322 http://hdl.handle.net/20.500.12105/8832 31527690 10.1038/s41598-019-49880-w 2045-2322 Scientific reports Mendelian randomization analysis rules out disylipidaemia as colorectal cancer cause