Claudia Agnoli1, Sara Grioni2, Sabina Sieri3, Carlotta Sacerdote4, Paolo Vineis5, Rosario Tumino6, Maria Concetta Giurdanella7, Valeria Pala8, Amalia Mattiello9, Paolo Chiodini10, Licia Iacoviello11, Amalia De Curtis12, Leonardo Cattaneo13, Fränzel J B van Duijnhoven14, Salvatore Panico15, Vittorio Krogh16. 1. Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy. Electronic address: claudia.agnoli@istitutotumori.mi.it. 2. Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy. Electronic address: sara.grioni@istitutotumori.mi.it. 3. Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy. Electronic address: sabina.sieri@istitutotumori.mi.it. 4. Center for Cancer Prevention (CPO-Piemonte), Via Santena 7, 10126 Turin, Italy; Human Genetics Foundation, Via Nizza 52, 10126 Turin, Italy. Electronic address: carlotta.sacerdote@cpo.it. 5. Human Genetics Foundation, Via Nizza 52, 10126 Turin, Italy; Imperial College of London, South Kensigton Campus, London SW7 2AZ, UK. Electronic address: p.vineis@imperial.ac.uk. 6. Cancer Registry, Department of Prevention, ASP 7, Via Dante 109, 97100 Ragusa, Italy. Electronic address: rtumino@tin.it. 7. Cancer Registry, Department of Prevention, ASP 7, Via Dante 109, 97100 Ragusa, Italy. Electronic address: giurda.regtumragusa@tiscali.it. 8. Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy. Electronic address: valeria.pala@istitutotumori.mi.it. 9. Department of Clinical and Experimental Medicine, University of Naples Federico II, Via Pansini 5, 80131 Naples, Italy. Electronic address: amattiel@unina.it. 10. Department of Mental and Physical Health and Preventive Medicine, Second University of Naples, Via Armanni 5, 80138 Naples, Italy. Electronic address: paolo.chiodini@unina.it. 11. Laboratory of Genetic and Environmental Epidemiology, Fondazione di Ricerca e Cura "Giovanni Paolo II", Catholic University, Largo Gemelli 1, 86100 Campobasso, Italy. Electronic address: licia.iacoviello@moli-sani.org. 12. Laboratory of Genetic and Environmental Epidemiology, Fondazione di Ricerca e Cura "Giovanni Paolo II", Catholic University, Largo Gemelli 1, 86100 Campobasso, Italy. Electronic address: amalia.decurtis@moli-sani.org. 13. Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy. Electronic address: cattaneo_leo@yahoo.com. 14. National Institute for Public Health and the Environment (RIVM), Antonie van Leeuwenhoeklaan 9, 3721 MA Bilthoven, The Netherlands; Division of Human Nutrition, Wageningen University, P.O. Box 8129, 6700 EV Wageningen, The Netherlands. Electronic address: franzel.van.duijnhoven@rivm.nl. 15. Department of Clinical and Experimental Medicine, University of Naples Federico II, Via Pansini 5, 80131 Naples, Italy. Electronic address: spanico@unina.it. 16. Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy. Electronic address: vittorio.krogh@istitutotumori.mi.it.
Abstract
BACKGROUND: Dyslipidemia is an established risk factor for many diseases, but its effect on colorectal cancer risk is less clear. We investigated the association of colorectal cancer risk with plasma triglycerides, total, HDL, and LDL cholesterol in four Italian EPIC centers. METHODS: We conducted a case-cohort study on participants recruited to four Italian EPIC centers (Turin, Varese, Naples, and Ragusa; 34,148 subjects). A random subcohort of 850 subjects was obtained and 286 colorectal cancer cases were diagnosed. Triglycerides, total and HDL cholesterol were determined in plasma samples obtained at baseline and stored at -196°C; LDL cholesterol was calculated. Hazard ratios (HR) with 95% confidence intervals (CI), adjusted for potential confounders, were estimated by Cox regression models using the Prentice method. RESULTS: The highest tertiles of total (HR 1.66, 95%CI 1.12-2.45) and LDL cholesterol (HR 1.87, 95%CI 1.27-2.76) were associated with increased colorectal cancer risk compared to lowest tertiles. Risks were greater for men than women, and for postmenopausal than premenopausal women. Highest tertiles of total and LDL cholesterol were also significantly associated with increased risks of colon cancer, distal colon cancer, and rectal cancer, but not proximal colon cancer. CONCLUSIONS: Our findings suggest that high levels of total and LDL cholesterol increase colorectal cancer risk, particularly in men and postmenopausal women. However additional studies are needed to clarify the role of plasma lipids in these cancers, particularly in view of the conflicting findings of previous studies.
BACKGROUND:Dyslipidemia is an established risk factor for many diseases, but its effect on colorectal cancer risk is less clear. We investigated the association of colorectal cancer risk with plasma triglycerides, total, HDL, and LDL cholesterol in four Italian EPIC centers. METHODS: We conducted a case-cohort study on participants recruited to four Italian EPIC centers (Turin, Varese, Naples, and Ragusa; 34,148 subjects). A random subcohort of 850 subjects was obtained and 286 colorectal cancer cases were diagnosed. Triglycerides, total and HDL cholesterol were determined in plasma samples obtained at baseline and stored at -196°C; LDL cholesterol was calculated. Hazard ratios (HR) with 95% confidence intervals (CI), adjusted for potential confounders, were estimated by Cox regression models using the Prentice method. RESULTS: The highest tertiles of total (HR 1.66, 95%CI 1.12-2.45) and LDL cholesterol (HR 1.87, 95%CI 1.27-2.76) were associated with increased colorectal cancer risk compared to lowest tertiles. Risks were greater for men than women, and for postmenopausal than premenopausal women. Highest tertiles of total and LDL cholesterol were also significantly associated with increased risks of colon cancer, distal colon cancer, and rectal cancer, but not proximal colon cancer. CONCLUSIONS: Our findings suggest that high levels of total and LDL cholesterol increase colorectal cancer risk, particularly in men and postmenopausal women. However additional studies are needed to clarify the role of plasma lipids in these cancers, particularly in view of the conflicting findings of previous studies.
Authors: Ji Yeon Kim; Yoon Suk Jung; Jung Ho Park; Hong Joo Kim; Yong Kyun Cho; Chong Il Sohn; Woo Kyu Jeon; Byung Ik Kim; Kyu Yong Choi; Dong Il Park Journal: World J Gastroenterol Date: 2016-04-07 Impact factor: 5.742