A Prospective Study of Dietary Polyunsaturated Fatty Acids and Colorectal Cancer Risk in Chinese Women

作者:Murff Harvey J*; Shu Xiao Ou; Li Honglan; Dai Qi; Kallianpur Asha; Yang Gong; Cai Hui; Wen Wanqing; Gao Yu Tang; Zheng Wei
来源:Cancer Epidemiology Biomarkers & Prevention, 2009, 18(8): 2283-2291.
DOI:10.1158/1055-9965.EPI-08-1196

摘要

In animal models of colon cancer, n-3 polyunsaturated fatty acids (PUFA) have antineoplastic properties, whereas n-6 PUFAs may promote carcinogenesis. Prior epidemiologic studies have been inconsistent regarding the association of PUFAs and colorectal cancer. We prospectively evaluated the association between PUFA intake and colorectal cancer in a cohort of 73,242 Chinese women who were interviewed in person at the baseline survey for the Shanghai Women';s Health Study. Dietary fatty acid consumption was derived using data collected from two food frequency questionnaires administered at baseline and 2 to 3 years later. The dietary total n-6 to n-3 PUFA ratio was strongly associated with colorectal cancer risk. Compared with women in the lowest quintile group, elevated relative risks (RR) were observed for the second [RR, 1.52; 95% confidence intervals (CI), 1.00-2.32], third (RR, 2.20; 95% CI, 1.41-3.45), fourth (RR, 1.65; 95% CI, 0.99-2.75), and fifth (RR, 1.95; 95% CI, 1.07-3.54) quintile groups. Arachidonic acid was associated with colorectal cancer risk with elevated RRs of 1.20(Q2-Q1) (95% CI, 0.87-1.64), 1.44(Q3-Q1) (95% CI, 1.05-1.98), 1.61(Q4-Q1) (95% CI, 1.17-2.23), and 1.39(Q5-Q1) (95% CI, 0.97-1.99; P(trend) = 0.03) with increasing dietary quintile. In a subset of 150 cancer cases and 150 controls, we found a statistically significant trend between an increasing n-6 to n-3 PUFA ratio and increasing production of prostaglandin E(2) (PGE(2)) as measured by urinary PGE(2) metabolites (P = 0.03). These results suggest that dietary PUFA and the ratio of n-6 to n-3 PUFA intake may be positively associated with colorectal cancer risk, and this association may be mediated in part through PGE(2) production. (Cancer Epidemiol Biomarkers Prev 2009;18(8):2283-91)