Xu Yao1, Zhong Tian2. 1. Department of General Surgery, Shengjing Hospital of China Medical University, 36, San Hao Street, Shenyang, Liaoning, 110004, People's Republic of China. 2. Department of General Surgery, Shengjing Hospital of China Medical University, 36, San Hao Street, Shenyang, Liaoning, 110004, People's Republic of China. zhongt_sjhospital@126.com.
Abstract
PURPOSE: The findings from epidemiologic studies of dyslipidemia and colorectal cancer risk have been conflicting. We performed a dose-response meta-analysis of published prospective studies to assess the aforementioned association. METHODS: Relevant studies that reported the association between the components of dyslipidemia (serum triglyceride, total cholesterol, and high-/low-density lipoprotein cholesterol) and colorectal cancer risk were identified by searching PubMed until the end of May 2014. We pooled the relative risks (RRs) from individual studies using a random- and fixed-effects models and performed dose-response, heterogeneity, and publication bias analyses. RESULTS: Seventeen prospective studies, including 1,987,753 individuals with 10,876 colorectal cancer events, were included in the meta-analysis. The overall pooled RR for high versus low concentrations for triglyceride (n = 9 studies) was 1.18 (95 % CI 1.04-1.34; I (2) = 47.8 %), for total cholesterol (n = 10 studies) was 1.11 (95 % CI 1.01-1.21; I (2) = 46.7 %), for high-density lipoprotein cholesterol (n = 6 studies) was 0.84 (95 % CI 0.69-1.02; I (2) = 42.5 %), and for low-density lipoprotein cholesterol (n = 3 studies) was 1.04 (95 % CI 0.60-1.81; I (2) = 82.7 %). In the dose-response analysis, the overall pooled RR was 1.01 (95 % CI 1.00-1.03; I (2) = 0 %) per 50 mg/dL of triglyceride and 1.01 (95 % CI 0.97-1.05; I (2) = 64.3 %) per 100 mg/dL of total cholesterol. CONCLUSIONS: This meta-analysis of prospective studies suggests that dyslipidemia, especially high levels of serum triglyceride and total cholesterol, is associated with an increased risk of colorectal cancer, whereas high-density lipoprotein cholesterol might associate with a decreased risk of colorectal cancer. Further studies are warranted to determine whether altering the concentrations of these metabolic variables may reduce colorectal cancer risk.
PURPOSE: The findings from epidemiologic studies of dyslipidemia and colorectal cancer risk have been conflicting. We performed a dose-response meta-analysis of published prospective studies to assess the aforementioned association. METHODS: Relevant studies that reported the association between the components of dyslipidemia (serum triglyceride, total cholesterol, and high-/low-density lipoprotein cholesterol) and colorectal cancer risk were identified by searching PubMed until the end of May 2014. We pooled the relative risks (RRs) from individual studies using a random- and fixed-effects models and performed dose-response, heterogeneity, and publication bias analyses. RESULTS: Seventeen prospective studies, including 1,987,753 individuals with 10,876 colorectal cancer events, were included in the meta-analysis. The overall pooled RR for high versus low concentrations for triglyceride (n = 9 studies) was 1.18 (95 % CI 1.04-1.34; I (2) = 47.8 %), for total cholesterol (n = 10 studies) was 1.11 (95 % CI 1.01-1.21; I (2) = 46.7 %), for high-density lipoprotein cholesterol (n = 6 studies) was 0.84 (95 % CI 0.69-1.02; I (2) = 42.5 %), and for low-density lipoprotein cholesterol (n = 3 studies) was 1.04 (95 % CI 0.60-1.81; I (2) = 82.7 %). In the dose-response analysis, the overall pooled RR was 1.01 (95 % CI 1.00-1.03; I (2) = 0 %) per 50 mg/dL of triglyceride and 1.01 (95 % CI 0.97-1.05; I (2) = 64.3 %) per 100 mg/dL of total cholesterol. CONCLUSIONS: This meta-analysis of prospective studies suggests that dyslipidemia, especially high levels of serum triglyceride and total cholesterol, is associated with an increased risk of colorectal cancer, whereas high-density lipoprotein cholesterol might associate with a decreased risk of colorectal cancer. Further studies are warranted to determine whether altering the concentrations of these metabolic variables may reduce colorectal cancer risk.
Authors: Henry Rodriguez-Broadbent; Philip J Law; Amit Sud; Kimmo Palin; Sari Tuupanen; Alexandra Gylfe; Ulrika A Hänninen; Tatiana Cajuso; Tomas Tanskanen; Johanna Kondelin; Eevi Kaasinen; Antti-Pekka Sarin; Samuli Ripatti; Johan G Eriksson; Harri Rissanen; Paul Knekt; Eero Pukkala; Pekka Jousilahti; Veikko Salomaa; Aarno Palotie; Laura Renkonen-Sinisalo; Anna Lepistö; Jan Böhm; Jukka-Pekka Mecklin; Nada A Al-Tassan; Claire Palles; Lynn Martin; Ella Barclay; Susan M Farrington; Maria N Timofeeva; Brian F Meyer; Salma M Wakil; Harry Campbell; Christopher G Smith; Shelley Idziaszczyk; Timothy S Maughan; Richard Kaplan; Rachel Kerr; David Kerr; Michael N Passarelli; Jane C Figueiredo; Daniel D Buchanan; Aung K Win; John L Hopper; Mark A Jenkins; Noralane M Lindor; Polly A Newcomb; Steven Gallinger; David Conti; Fred Schumacher; Graham Casey; Lauri A Aaltonen; Jeremy P Cheadle; Ian P Tomlinson; Malcolm G Dunlop; Richard S Houlston Journal: Int J Cancer Date: 2017-04-06 Impact factor: 7.316